Despite its crucial role in interventional therapies for liver malignancy, cone-beam computed tomography (CBCT) has not yet been fully integrated into clinical practice due to several complicating factors, including nonstandardized operations and limited recognition of CBCT among interventional radiologists. In response, the Chinese College of Interventionalists has released a consensus statement aimed at standardizing and promoting the application of CBCT in the interventional therapies for liver malignancy. This statement summarizes CBCT scanning techniques, and operational standards, and highlights its potential applications in clinical practice.

Yersinia pseudotuberculosis (Yptb) causes intestinal infection and can spread to the liver, where the bacterium induces hemosiderosis, abscesses, and hepatitis. To evade the immune response of the host organism, Yptb expresses at least six plasmid-encoded Yersinia outer proteins belonging to the Type III secretion system, which suppress phagocytic activity. Recently, evidence has accumulated that chromosome-encoded protein toxins are also involved in the anti-phagocytic defense of Yptb. Most of these toxins have been found in isolates from patients with Far East scarlet-like fever, often accompanied by liver pathology. Yersinia proteins contribute to bacterial colonization of lymphoid organs through their effects on immune cells. A thorough understanding of the immunomodulatory effects of these toxic proteins on bacterial dissemination and colonization in the liver will contribute to the development of novel approaches to cure hepatic pathology during Yptb infection. The review aimed to summarize the current data on the mechanisms of effects of Yptb plasmid- and chromosome-encoded toxins on bacterial colonization in the liver. The review highlights the fine-tuning of immune system activity by toxins encoded by both a 70-kb plasmid and chromosomes, through various mechanisms of action of individual proteins and their interactions. The focus is on mechanisms that promote bacterial survival in macrophages, including those that facilitate bacterial-induced macrophage polarization towards the M2 phenotype. The role of a type of phagocyte death in bacterial dissemination and colonization in the organs is also discussed.

Acute liver failure (ALF) is a life-threatening clinical problem with limited treatment options. Administration of human umbilical cord mesenchymal stem cells (hUC-MSCs) may be a promising approach for ALF. This study aimed to explore the role of hUC-MSCs in the treatment of ALF and the underlying mechanisms.

A mouse model of ALF was induced by lipopolysaccharide and d-galactosamine administration. The therapeutic effects of hUC-MSCs were evaluated by assessing serum enzyme activity, histological appearance, and cell apoptosis in liver tissues. The apoptosis rate was analyzed in AML12 cells. The levels of inflammatory cytokines and the phenotype of RAW264.7 cells co-cultured with hUC-MSCs were detected. The C-Jun N-terminal kinase/nuclear factor-kappa B signaling pathway was studied.

The hUC-MSCs treatment decreased the levels of serum alanine aminotransferase and aspartate aminotransferase, reduced pathological damage, alleviated hepatocyte apoptosis, and reduced mortality in vivo. The hUC-MSCs co-culture reduced the apoptosis rate of AML12 cells in vitro. Moreover, lipopolysaccharide-stimulated RAW264.7 cells had higher levels of tumor necrosis factor-α, interleukin-6, and interleukin-1β and showed more CD86-positive cells, whereas the hUC-MSCs co-culture reduced the levels of the three inflammatory cytokines and increased the ratio of CD206-positive cells. The hUC-MSCs treatment inhibited the activation of phosphorylated (p)-C-Jun N-terminal kinase and p-nuclear factor-kappa B not only in liver tissues but also in AML12 and RAW264.7 cells co-cultured with hUC-MSCs.

hUC-MSCs could alleviate ALF by regulating hepatocyte apoptosis and macrophage polarization, thus hUC-MSC-based cell therapy may be an alternative option for patients with ALF.

Herpetic Epithelial Keratitis is characterized by a corneal dendritic lesion, and prolonged or recurrent medication such as acyclovir, raises the possibility of resistant strains, necessitating the search for new therapies. An 84-year-old woman, phototype III, reported severe discomfort in the left eye. The presence of a dendritic ulcer was confirmed. Acyclovir therapy (oral—1.6 g/day and topical—seven days) was initiated and replaced by famciclovir (oral–1.5 g/day—seven days; topical acyclovir discontinued). Every three months, a new recurrence occurred. Famciclovir treatment (seven days) was subsequently supplemented with L-lysine (3 g—loading dose + 500 mg/day per 30 days) with L-arginine intake control. After amino acid supplementation, the clinical signs of the active lesion were reduced compared to previous treatment. Furthermore, a longer interval between recurrences was observed until they ultimately stopped. The patient is controlling L-arginine intake. When necessary, L-lysine supplementation is associated. Additional investigation is needed on the proposed supplementary therapy for Herpetic Epithelial Keratitis, which could help reduce side effects and resistance to antiviral drugs. However, as documented in this case report, amino acid supplementation can be recommended for controlling herpesvirus infection with no risk of adverse effects

Recent therapeutic advances for gastrointestinal tract tumors have focused on targeted therapies and molecular profiling. Anti-human epidermal growth factor receptor (HER) 2 drugs, claudin 18.2 inhibitors, and immune checkpoint inhibitors have shown efficacy in small subgroups of gastric, esophageal, and colorectal cancers, respectively. However, their benefits remain limited, and small bowel carcinomas continue to lack effective treatments. Conventional chemoradiation remains the primary approach for most cases. The future development of therapies for these cancers will depend on understanding the molecular basis of the diseases. This review aims to summarize the main breakthroughs in the knowledge of the molecular basis of gastrointestinal cancers, focusing on those that could lead to significant changes in the management and prognosis of these prevalent and still lethal neoplasms.

Over the course of the COVID-19 pandemic and its aftermath, growing concerns have emerged about the mental health of children and youth. Disease, loss, and lockdowns presented young people with enormous stressors, and much research suggests elevated levels of pediatric depression, anxiety, suicidality, and obsessive-compulsive behavior. However, considerable debate remains about the nature and persistence of these symptoms. This narrative review, conducted approximately four years after the onset of the pandemic, summarizes the major findings from four years of research, including empirical studies, meta-analyses, and systematic reviews. Studies were sourced from scholarly databases using the keywords “COVID-19”, “children”, “adolescents”, and “mental health”. The existing literature on the prevalence of depression in youth indicated that worldwide rates varied from 2.2% to 11.8% of the population, with one study revealing that one in four young people reported depressive symptoms. More specifically, 44% of youth in the United States demonstrated depression, while in China, the prevalence rate ranged from 11% to 44% of young people. Reviewed data showed that 20% of youth globally endorsed symptoms of anxiety or stress reactions, with countries such as Denmark (44%), Canada (45%), and the United States (32%) reporting extremely high rates. In the implications section, recommendations for screening and intervention procedures are outlined.

Hepatitis B virus (HBV) infection is a major risk factor for cirrhosis and liver cancer, and its treatment continues to be difficult. We previously demonstrated that a dopamine analog inhibited the packaging of pregenomic RNA into capsids. The present study aimed to determine the effect of dopamine on the expressions of hepatitis B virus surface and e antigens (HBsAg and HBeAg, respectively) and to elucidate the underlying mechanism.

We used dopamine-treated HBV-infected HepG2.2.15 and NTCP-G2 cells to monitor HBsAg and HBeAg expression levels. We analyzed interferon-stimulated gene 15 (ISG15) expression in dopamine-treated cells. We knocked down ISG15 and then monitored HBsAg and HBeAg expression levels. We analyzed the expression of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway factors in dopamine-treated cells. We used dopamine hydrochloride-treated adeno-associated virus/HBV-infected mouse model to evaluate HBV DNA, HBsAg, and HBeAg expression. HBV virus was collected from HepAD38.7 cell culture medium.

Dopamine inhibited HBsAg and HBeAg expression and upregulated ISG15 expression in HepG2.2.15 and HepG2-NTCP cell lines. ISG15 knockdown increased HBsAg and HBeAg expression in HepG2.2.15 cells. Dopamine-treated cells activated the JAK/STAT pathway, which upregulated ISG15 expression. In the adeno-associated virus-HBV murine infection model, dopamine downregulated HBsAg and HBeAg expression and activated the JAK-STAT/ISG15 axis.

Dopamine inhibits the expression of HBsAg and HBeAg by activating the JAK/STAT pathway and upregulating ISG15 expression.

Chronic cholestasis due to heritable causes is usually diagnosed in childhood. However, many cases can present and survive into adulthood. The time course varies considerably depending on the underlying etiology. Laboratory data usually reveal elevated conjugated hyperbilirubinemia, alkaline phosphatase, and gamma-glutamyl transpeptidase. Patients may be asymptomatic; however, when present, the typical symptoms are pruritus, jaundice, fatigue, and alcoholic stools. The diagnostic methods and management required depend on the underlying etiology. The development of genome-wide associated studies has allowed the identification of specific genetic mutations related to the pathophysiology of cholestatic liver diseases. The aim of this review was to highlight the genetics, clinical pathophysiology, presentation, diagnosis, and treatment of heritable etiologies of chronic cholestatic liver disease.

The quantitative effects of alcohol consumption on cirrhosis and hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) infection are unknown. This study aimed to establish a dose-dependent model of alcohol consumption on the risks of cirrhosis and HCC.

PubMed, Embase, the Cochrane Library, Web of Science, and four Chinese databases were searched for studies published from their inception to 15 May 2024. A random-effects model was used to pool the data on the incidence of cirrhosis and HCC, and a dose-dependent model of alcohol’s effect on cirrhosis and HCC was established.

A total of 33,272 HBV patients from 45 studies were included. Compared with non-drinkers, the overall pooled odds ratio (OR) for cirrhosis was 2.61 (95% confidence interval [CI]: 1.46–4.66; I2 = 94%, p < 0.001), and the OR for HCC was 2.27 (95% CI: 1.50–3.43; I2 = 90%, p < 0.001) among drinkers. Compared with low-level drinkers, the estimated pooled OR for cirrhosis was 2.34 (95% CI: 1.59–3.44; I2 = 87%, p < 0.001), and the OR for HCC was 2.42 (95% CI: 1.90–3.09; I2 = 80%, p < 0.001) among high-level drinkers. Furthermore, a linear dose-dependent analysis showed that each daily consumption of 12 g of alcohol increased the risk of cirrhosis by 6.2% and the risk of HCC by 11.5%.

Alcohol dose-dependently increases the risks of cirrhosis and HCC in patients with HBV infection, and patients with daily alcohol consumption of more than 12 g should be strictly monitored.

Hepatocellular carcinoma (HCC) cases with small nodules are commonly treated with radiofrequency ablation (RFA), but the recurrence rate remains high. This study aimed to establish a blood signature for identifying HCC with metastatic traits pre-RFA.

Data from HCC patients treated between 2010 and 2017 were retrospectively collected. A blood signature for metastatic HCC was established based on blood levels of alpha-fetoprotein and des-γ-carboxy-prothrombin, cell-free DNA (cfDNA) mutations, and methylation changes in target genes in frozen-stored plasma samples that were collected before RFA performance. The HCC blood signature was validated in patients prospectively enrolled in 2021.

Of 251 HCC patients in the retrospective study, 33.9% experienced recurrence within 1 year post-RFA. The HCC blood signature identified from these patients included des-γ-carboxy-prothrombin ≥40 mAU/mL with cfDNA mutation score, where cfDNA mutations occurred in the genes of TP53, CTNNB1, and TERT promoter. This signature effectively predicted 1-year post-RFA recurrence of HCC with 92% specificity and 91% sensitivity in the retrospective dataset, and with 87% specificity and 76% sensitivity in the prospective dataset (n=32 patients). Among 14 cases in the prospective study with biopsy tissues available, positivity for the HCC blood signature was associated with a higher HCC tissue score and shorter distance between HCC cells and microvasculature.

This study established an HCC blood signature in pre-RFA blood that potentially reflects HCC with metastatic traits and may be valuable for predicting the disease’s early recurrence post-RFA.