Cell cycle checkpoint-related genes (CCCRGs) are implicated in the development and progression of hepatocellular carcinoma (HCC). However, their precise roles and underlying mechanisms remain insufficiently characterized and require further investigation. This study aimed to explore the prognostic significance of CCCRGs in HCC, and to investigate the mechanism by which they promote the progression of HCC.

HCC datasets from The Cancer Genome Atlas and International Cancer Genome Consortium were analyzed to identify hub genes. A prognostic model was constructed and validated using Kaplan–Meier analysis, nomogram, calibration curves, decision curve analysis, and receiver operating characteristic analysis. Immune infiltration patterns were assessed using single sample gene set enrichment analysis, while pathway activities were evaluated via gene set variation analysis. Single-cell RNA sequencing data from GSE149614 were analyzed with Seurat and CellChat to investigate cell–cell communication. Patient-derived HCC specimens were examined through immunohistological evaluation, HCC cell lines were used for in vitro functional assays, and in vivo tumor growth was assessed through animal experiments.

CCCRGs showed significant associations with prognosis, malignant biological behavior, and immune responses in HCC. Centromere protein (CENP) I was identified as a critical hub gene that markedly promoted HCC proliferation, metastasis, and epithelial–mesenchymal transition, while inhibiting apoptosis. Mechanistically, CENPI suppressed YAP phosphorylation, enhancing its nuclear translocation and thereby driving malignant progression. Additionally, CENPI impaired immune effector cell infiltration, likely by disrupting tumor antigen presentation and chemokine-mediated CD8+ T cell chemotaxis, thereby promoting immune escape.

This study underscores the prognostic significance of CCCRGs in HCC and identifies CENPI as a key driver of tumor progression through the Hippo pathway. Furthermore, it reveals CENPI’s role in promoting immune escape, suggesting novel therapeutic targets for HCC treatment.

Empirical and theoretical studies can be distinguished among the areas of investigation of the renin-angiotensin-aldosterone system (RAAS) and its relationship with the development of cardiovascular diseases. Theoretical work is based mainly on the bioinformatic analysis of key elements of RAAS (genes, proteins, metabolites), on calculations and predictions of protein interactions, and on mechanisms of RAAS gene expression regulation. An associative gene network based on big data analysis allows us to reveal relationships among the proteins, regulatory pathways, and biological processes acting in RAAS, as well as to identify new diagnostic markers, therapeutic targets, putative molecular mechanisms of the development of RAAS-associated diseases, drug interactions, and drug toxicity.

The reconstruction and analysis of associative gene networks were performed using ANDSystem. The regulation of RAAS-associated gene expression was analyzed by transcription factor (TF) binding sites (TFBSs) prediction in the proximal promoters of these genes and by studying interactions between TFs themselves using the Ensembl Biomart web service and AnimalTFDB 4.0. The recognition of potential TFBSs in RAAS gene promoters was performed using MoLoTool.

According to the centrality criteria of the RAAS associative gene network, the following proteins were identified as exerting a significant influence on information interplay between network components: IL6, EDN1, TNFA, MK01, LEP, and JUN. Analysis of the ten identified TFs and their TFBSs among the genes in the RAAS network under study revealed clusters of three to 26 genes regulated by them.

Components with the highest values of centrality and vertex degrees were identified in the reconstructed associative gene network of the RAAS, and ten TFs supposed to regulate 26 RAAS genes were determined.

Perioperative anaphylaxis is a rare, life-threatening, iatrogenic condition that predominantly arises following anesthesia. The unique context of this condition, characterized by the concurrent administration of multiple drugs, patient draping, and altered physiological states, presents significant diagnostic and therapeutic challenges, contributing to a higher mortality rate compared to anaphylaxis in other settings. This narrative review synthesizes the evidence to delineate the evolving etiology, pathophysiology, atypical clinical presentation, evidence-based immediate management, and strategic prevention of perioperative anaphylactic reactions. The primary causative agents include neuromuscular blocking agents, antibiotics, and latex, with emerging culprits such as chlorhexidine, dyes, and novel agents like remimazolam. Diagnosis is complicated by the paucity of cutaneous signs; thus, cardiovascular collapse combined with a low end-tidal carbon dioxide level has emerged as a useful supportive diagnostic indicator that requires integration with the clinical context. Immediate management prioritizes the prompt administration of epinephrine and aggressive fluid resuscitation. Subsequent allergological investigations, primarily via skin testing and serum tryptase/histamine measurement, are paramount for identifying the causative agent and preventing its recurrence. Prevention strategies emphasize meticulous history-taking, risk stratification, and the creation of latex-free environments. Future directions must focus on establishing global surveillance networks, exploring novel biomarkers and risk factors such as the circulating microbiome—a preliminary but promising area of research—and enhancing team preparedness through simulation training to improve patient safety outcomes.

Breast cancer (BCA) is one of the most common cancers worldwide, with a high rate of incidence and mortality. This review provides global information on BCA therapy using curcumin. Chemotherapy, as an effective treatment for different stages of BCA, and curcumin, generally regarded as safe compound and an alternative to synthetic drugs, have been described for the treatment of BCA. A few parameters, including nano-curcumin versus bulk curcumin and its encapsulated form versus its corresponding free form, have been discussed. Curcumin, a safe and edible compound with antitumor properties, is a promising medicinal compound for the treatment of BCA. Encapsulation of curcumin enhances its stability and anticancer efficiency. Nano-curcumin exhibits superior properties when compared to its bulk counterparts, leading to notable interactions and effects.

This review aims to advocate for a paradigm shift in herbal safety by proposing a cohesive molecular framework that integrates advanced “omics” technologies with artificial intelligence (AI) to address the clinical challenges of herb-induced liver injury (HILI). Traditional herbal medicine constitutes a substantial, yet often unregulated, component of global healthcare, driving high patient exposure alongside a significant and escalating clinical burden of HILI. Current pharmacovigilance systems are critically undermined by fundamental deficits, including severe underreporting, unknown population denominators, and pervasive product quality failures. Furthermore, the complexity of multi-ingredient formulations and the frequency of herb-drug interactions complicate causality assessment, particularly for high-risk drugs. To bridge the gap between empirical practice and contemporary safety standards, this integrated “omics”-AI paradigm transforms herbal safety from a reactive, population-level assessment into an evidence-based, personalized system. By enabling precise risk mitigation, this approach establishes a scientifically rigorous foundation for the future of integrative liver health. In conclusion, the synergy of molecular profiling and computational intelligence provides the necessary tools to modernize herbal pharmacovigilance, ensuring that traditional wisdom is effectively harmonized with modern technological standards for enhanced patient safety.

Acromegaly requires multimodal management. While surgery is first-line, many patients have persistent/recurrent disease. Gamma knife radiosurgery (GKRS) offers precise radiation, but data on its use as initial therapy remain limited. This study aimed to review the outcomes and report on our experience in treating patients with acromegaly using initial GKRS.

We retrospectively identified 33 patients with acromegaly who underwent GKRS from 1993 until 2016 at the Department of Radiotherapy, the Second Affiliated Hospital of Guangzhou Medical University. These patients had complete endocrine, radiological, and imaging data before and after GKRS. Furthermore, univariate and multivariate analysis was utilized to analyze the potential prognostic factors of endocrine remission and new-onset hypopituitarism.

Thirty-three patients were enrolled in the study. Fifteen patients (45.5%) were males and 18 (54.5%) were females. The median age was 44.0 years (range, 24.9–66.2 years). During a median follow-up of 65.6 months (range, 12.9–297.6), the median margin dose for GKRS was 15.0 Gy (range, 10.8–20.3 Gy). Endocrine remission was achieved in nine of the 33 patients (27.3%) over a mean follow-up of 85.1 months (range, 12.9–161.3). No prognostic factors demonstrated a significant association with endocrine remission. New-onset hypopituitarism occurred in eight patients (24.2%) after GKRS. The tumor control rate was 100%. Only one patient developed worsening visual dysfunction. No new cranial neuropathy was noted.

Initial GKRS for acromegaly provided effective tumor control and partial endocrine remission with a favorable safety profile, notably a low rate of new-onset hypopituitarism, representing a viable treatment option.

Metaplastic breast carcinoma, a rare entity (<1% of breast neoplasms), lacks comprehensive spectroscopic characterization. This study aimed to address this gap by providing a qualitative and quantitative spectroscopic profile of metaplastic carcinoma in comparison to ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC).

A retrospective analysis was conducted on archival tissue blocks of metaplastic carcinoma (n = 10), DCIS (n = 12), and IDC (n = 31). Sections were stained with hematoxylin and eosin for histological confirmation. Attenuated total reflectance Fourier-transform infrared spectroscopy was performed on adjacent unstained sections, with normal breast tissue (n = 10) serving as the control. Spectral data were analyzed using t-tests to identify significant differences in peak intensities and ratios. Hierarchical clustering analysis and receiver operating characteristic curves were generated to assess the diagnostic potential of selected spectral features.

Spectral analysis revealed that mean peak intensities were generally lower in all carcinoma subtypes compared to normal breast tissue. Specific ratios, including A1237/A1080 (phosphate; p < 0.01), A1043/1543 (glycogen; p < 0.01), and A1080/A1632 (nucleocytoplasmic index; p < 0.03), were significantly elevated in carcinomatous tissues. Receiver operating characteristic analysis identified peak 3,280 (area under the curve (AUC) = 0.93–0.96) as highly effective in differentiating normal from carcinomatous tissues. Peak 2,922 showed specificity for distinguishing normal tissue from IDC (AUC ≈ 0.7). Peak 1,744 effectively discriminated between DCIS and metaplastic carcinoma (AUC = 0.7). The ratio 1,080/1,632 (nucleocytoplasmic ratio) demonstrated exceptional diagnostic accuracy, distinguishing normal from carcinomatous tissues (AUC ≈ 1.0), DCIS from IDC (AUC ≈ 0.86), and DCIS from metaplastic carcinoma (AUC ≈ 0.8).

Attenuated total reflectance Fourier-transform infrared spectroscopy, particularly using peak 3,280 (Amide A) and the 1,080/1,632 ratio (nucleocytoplasmic index), offers a promising approach for discriminating between normal breast tissue and carcinoma, as well as differentiating pre-IDC from metaplastic carcinoma. These spectral markers demonstrate both statistical significance and diagnostic potential.

Primary biliary cholangitis (PBC) is a chronic cholestatic disorder in which symptoms exert a direct influence on patients’ quality of life. Beyond pruritus and fatigue, patients with PBC are also prone to developing osteoporosis (OP). This skeletal condition not only heightens the likelihood of fractures but is also associated with elevated mortality. With the overall prevalence of PBC rising, a parallel increase in OP incidence among these patients can be anticipated. Early recognition, preventive strategies, and appropriate therapeutic approaches are essential for preserving patients’ quality of life. Nevertheless, current data on the management of OP in PBC remain limited. Most existing recommendations are extrapolated from studies on postmenopausal OP. However, these findings have not been effectively adapted into practical management protocols for PBC-related OP, largely due to distinct pathophysiological mechanisms between the two conditions. The absence of well-established preventive and therapeutic measures continues to represent a major obstacle in addressing OP among patients with PBC. This review offers a detailed synthesis of the epidemiology, underlying mechanisms, and therapeutic considerations of OP linked to PBC.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a major global health concern and encompasses a spectrum ranging from hepatic steatosis and metabolic dysfunction-associated steatohepatitis to liver fibrosis, cirrhosis, and ultimately hepatocellular carcinoma. Insulin resistance, the pathogenic cornerstone of MASLD, drives enhanced peripheral lipolysis and increased hepatic de novo lipogenesis, thereby overloading the liver with lipids and inducing steatosis. Subsequent lipotoxicity, inflammation, and gut microbiota dysbiosis further exacerbate disease progression. The gut microbiota and their metabolites communicate with the liver via the gut-liver axis, forming a complex signaling network that directly or indirectly modulates hepatic metabolism, systemic immune responses, oxidative stress, and intestinal barrier integrity. In this review, we synthesize evidence for the beneficial and detrimental effects of the major human gut microbial communities and their metabolites during the course of MASLD. We delineate how these gut-derived factors regulate hepatic function through an integrated tripartite “gut-liver axis–oxidative stress–metabolic reprogramming” mechanism. These insights may inform microbiome-based precision interventions and accelerate the development of therapeutic strategies targeting MASLD.