Gut dysbiosis has been reported in severe liver diseases. However, information on the impact of hepatitis E virus infection on the gut microbiota, and the association between enteric microbiota disturbances and acute hepatitis E (AHE), is limited, particularly in elderly patients with AHE (AHE-elderly). Our objective was to characterize the AHE-specific microbiome in elderly patients and evaluate its association with clinical outcomes.

Fecal samples and clinical data were collected from 58 AHE-elderly patients (46 self-healing cases, 12 non-self-healing cases) and 30 elderly patients with healthy controls (hereinafter referred to as HCs-elderly). Gut microbiota composition was analyzed using 16S rRNA gene sequencing. Bioinformatic analyses, including alpha diversity and STAMP, were performed. The predictive potential of Bacteroides fragilis was assessed using statistical analysis and receiver operating characteristic curves.

Alpha diversity indices showed no significant differences in microbial diversity between the AHE-elderly and HCs-elderly groups, nor between self-healing and non-self-healing groups among AHE-elderly patients. Nevertheless, a trend toward altered species richness was observed. In the AHE-elderly group, the relative abundance of Firmicutes, Lactobacillales, and Bacilli increased significantly. Meanwhile, compared with the self-healing group, Bacteroidetes were more abundant in the non-self-healing group. At the species level, Bacteroides fragilis was the most abundant in the non-self-healing group, significantly contributing to the divergence in gut microbiota between the two groups.

The relative abundance of Bacteroidetes significantly distinguished AHE-elderly patients from healthy controls and could more accurately predict recovery outcomes in elderly AHE patients. These findings suggest new strategies for preventing and managing AHE recurrence in the elderly patients.

Liquid biopsy (LB) represents a promising strategy for the early diagnosis and treatment of lung cancer. However, relying solely on single-biomarker immunohistochemistry for predictive purposes has shown limited efficacy, often leading to suboptimal responses in certain patients. LB provides a complementary or alternative approach to immunohistochemistry by aiding in the identification of patients better suited for immunotherapy, thereby improving treatment precision. This review highlights key LB targets, including circulating tumor cells, exosomes, and small protein molecules, and explores the predictive and prognostic value of LB in immunotherapy for lung cancer and other tumors. These biomarkers play complex and multifaceted roles in liquid biopsies. Consequently, researchers have developed numerous targeted detection methods to study and identify key factors among multiple biomarkers in lung cancer and other tumor diseases. In addition, the limitations and future directions of LB are examined, aiming to advance its clinical application and support the development of personalized and precise immunotherapy. The integration of LB with artificial intelligence holds significant clinical potential for guiding immunotherapy and advancing precision medicine in lung cancer and other tumors.

Gastrointestinal complications are common in patients after ischemic stroke. Gastric motility is regulated by gastric pace-making activity (also called gastric myoelectrical activity (GMA)) and autonomic function. The aim of this study was to evaluate GMA, assessed by noninvasive electrogastrography (EGG), and autonomic function, measured via spectral analysis of heart rate variability derived from the electrocardiogram in patients with ischemic stroke.

EGG and electrocardiogram were simultaneously recorded in both fasting and postprandial states in 14 patients with ischemic stroke and 11 healthy controls. Multi-channel surface EGG was used to measure GMA, and autonomic function was evaluated by heart rate variability spectral analysis.

Compared to healthy subjects, patients with ischemic stroke, especially those with a modified Rankin scale ≥ 4, had impaired GMA in both fasting and postprandial states. This included a lower percentage of normal gastric slow waves (the basic rhythmic waves of GMA) and a higher percentage of tachygastria, bradygastria, or arrhythmia. Patients with ischemic stroke also showed a decrease in the dominant frequency and power of the gastric slow waves. Autonomic functions were altered in ischemic stroke patients with a modified Rankin scale ≥ 4, as reflected by increased sympathetic activity and reduced parasympathetic activity.

Gastric pace-making activity is impaired in patients with severe ischemic stroke, as evidenced by a reduced percentage of normal gastric slow waves and a lower frequency of gastric slow waves, likely due to impaired autonomic functions.

Artificial intelligence (AI) is profoundly transforming the paradigm of solid tumor drug development. By integrating multi-omics data, spatial transcriptomics, and advanced computational models, AI has significantly accelerated the discovery and validation of new targets, compressing the traditional ten-year research and development cycle to two to three years. Generative AI platforms have optimized small molecule inhibitors, biologics, and messenger RNA vaccines, achieving breakthroughs in overcoming tumor heterogeneity, improving efficacy, and predicting drug resistance. However, clinical translation still faces challenges such as data bias, algorithm transparency, and the validation gap between models and real-world human experience. This review aims to systematically elaborate on the transformative role of AI in solid tumor drug development and to promote interdisciplinary cooperation as well as the construction of ethical frameworks to enable the full realization of precision oncology.

Atypical teratoid/rhabdoid tumor (AT/RT) is a rare and highly aggressive embryonal tumor that predominantly affects infants and young children. This malignancy arises from primitive neuroectodermal cells and exhibits heterogeneous differentiation into various embryonic tissues. Due to its rarity and complexity, diagnosing and managing AT/RT present significant challenges. Recent studies have summarized the key features of cerebellar and supratentorial AT/RT cases; however, critical gaps remain in understanding their diffuse leptomeningeal variants and long-term functional outcomes. Here, we report a case of a two-year-old child diagnosed with cerebellar AT/RT, who presented with vomiting and gait instability. The patient underwent a gross total resection followed by adjuvant radiotherapy and chemotherapy. Despite achieving radiological remission, the patient survived for only eight months and experienced severe neurological deficits, including persistent ataxia and recurrent infections. This case highlights the disconnect between surgical success and long-term quality of life. It underscores the importance of integrating molecular diagnostics and palliative care to address the multifaceted burden of AT/RT.

The importance of putative folate-biopterin metabolic interactions lies in the role they may play in the expression of several clinically relevant phenotypes. However, to date, clinical studies on folate-biopterin interactions have been limited. The purpose of this article was to highlight the close relationship between these two cofactors, which share structural similarities and exhibit overlapping metabolic pathways. This folate-biopterin crosstalk has generated several ideas and hypotheses that are critical to advancing the biochemical understanding of several important and seemingly disparate clinical and/or biologically important phenotypes. These phenotypes include melanization/pigmentation, phenylketonuria, autism, neural tube defects, affective disorders, and vascular disease. This review provides a timely, integrated overview of this important area of biochemistry, which is under-represented in the literature and would benefit from further scientific and clinical investigation using improved metabolite-specific analytical methodologies applied to clinically relevant questions.

Metabolic dysfunction-associated fatty liver disease, representing a spectrum of liver disorders from simple steatosis to metabolic dysfunction-associated steatohepatitis, fibrosis, and cirrhosis, has emerged as one of the most prevalent chronic liver conditions globally, affecting an estimated approximately 30% of the world's population. Its pathogenesis is highly complex, involving intricate interactions between genetic predisposition, metabolic dysregulation, inflammation, and cellular stress responses. Within this complex landscape, orphan nuclear receptors (ONRs) have gained significant attention. Defined by the lack of identified endogenous ligands, ONRs function as master transcriptional regulators controlling diverse biological processes. Crucially, they play pivotal roles in the development and progression of numerous diseases, including metabolic disorders.This review specifically focuses on elucidating the critical contributions of various ONRs to the pathogenesis of metabolic dysfunction-associated fatty liver disease. We examined how these receptors modulate key pathological drivers: lipid metabolism, inflammation,and autophagy.

Ginseng, a traditional Chinese medicinal herb, has been used for centuries to enhance vitality and overall well-being. This review synthesizes multiple studies to summarize the latest discoveries on the immunoregulatory effects of ginseng, its role in improving patients’ quality of life, and new evidence of its antitumor properties. It concludes that ginseng and its extracts can improve patients’ quality of life and may have the potential to target tumor cells. Meanwhile, ginseng extracts significantly improve sub-health status, with an 85% improvement rate observed in young adults after 30 days of intervention. This review provides valuable new evidence for ongoing research on ginseng and its extracts.

Breast cancer is one of the leading causes of mortality among women worldwide. Tumor necrosis factor α-induced protein 3-interacting protein 1 (TNIP1) is a ubiquitin-binding protein that is widely expressed, but its function in breast cancer cells remains unknown. This study aimed to elucidate the molecular mechanism of TNIP1 regulation in the proliferation and apoptosis of breast cancer cells.

A colony formation assay was conducted on MCF-7 and T47D cells stably transfected with TNIP1/cyclin G1 (CCNG1) short hairpin RNAs. Quantitative polymerase chain reaction was performed to assess the relative abundances of TNIP1, CCNG1, and cyclin D1 (CCND1) messenger RNAs. Immunoprecipitation and immunoblotting were used to detect the expression of TNIP1, CCNG1, CCND1, and related proteins. A dual-luciferase reporter assay was employed to explore the molecular mechanism of TNIP1 in signal transduction. Caspase activity in MCF-7 and T47D cells transfected with TNIP1 short hairpin RNAs was measured using the Caspase-Glo 3/7 assay.

Ablation of TNIP1 induced growth arrest in breast cancer cells. TNIP1 directly interacted with CCNG1, and TNIP1 knockdown increased the ubiquitination of CCNG1. CCNG1 knockdown also induced growth arrest in MCF-7 and T47D cells. Furthermore, TNIP1 knockdown activated the NF-κB pathway and induced apoptosis in these cells.

TNIP1 regulates the proliferation and apoptosis of breast cancer cells, suggesting that TNIP1 may serve as a potential biomarker for breast cancer.

Chronic hepatitis B virus (HBV)-infected patients may exhibit liver fibrosis and other pathological changes despite normal alanine aminotransferase (ALT). This study aimed to assess the efficacy and safety of tenofovir amibufenamide (TMF) in chronic HBV-infected patients with normal ALT levels.

The ongoing PROMOTE study (NCT05797714) is the first prospective, multicenter, randomized, open-label, blank-controlled clinical trial involving chronic HBV-infected patients with normal ALT levels. Participants were randomized in a 1:1 ratio to receive either TMF (TMF group) or no treatment (blank control group). The primary efficacy endpoint was the proportion of participants achieving HBV DNA levels <20 IU/mL at 48 weeks.

A total of 197 participants were enrolled, with 95 in the TMF group and 102 in the blank control group. At 48 weeks, a significantly greater proportion of participants in the TMF group achieved HBV DNA levels <20 IU/mL compared with the control group (74.2% vs. 9.0%, P < 0.001). The TMF group demonstrated more pronounced reductions in HBV DNA (−2.63 vs. −0.22 log10 IU/mL, P < 0.001), HBsAg (−0.07 vs. −0.04 log10 IU/mL, P = 0.02), and ALT levels (−14.09% vs. 0%, P = 0.003) compared with the blank control. In the TMF group, the proportion of participants with high-normal ALT levels (20–40 IU/L) was reduced. No significant differences were observed between the groups in creatinine, glomerular filtration rate, bone turnover biomarkers, lipid profiles, or phosphorus levels.

TMF treatment demonstrates significant efficacy in chronic HBV-infected patients with normal ALT levels and shows a favorable safety profile regarding bone, renal, and lipid parameters. The PROMOTE study is ongoing, and further results at 96 and 144 weeks are expected to provide additional insights.