A study on construction of a prognosis model for liver cancer based on analgesic targets and screening therapeutic drugs.

BACKGROUND: Liver cancer is one of the most malignant liver diseases in the world, and the 5-year survival rate of such patients is low. Analgesics are often used to cure pain prevalent in liver cancer. The expression changes and clinical significance of the analgesic targets (ATs) in liver cancer have not been deeply understood. OBJECTIVE: The purpose of this study is to clarify the expression pattern of ATs gene in liver cancer and its clinical significance. Through the comprehensive analysis of transcriptome data and clinical parameters, the prognosis model related to ATs gene is established, and the drug information sensitive to ATs is mined. METHODS: The study primarily utilized transcriptomic data and clinical information from liver cancer patients sourced from The Cancer Genome Atlas (TCGA) database. These data were employed to analyze the expression of ATs, conduct survival analysis, gene set variation analysis (GSVA), immune cell infiltration analysis, establish a prognostic model, and perform other bioinformatic analyses. Additionally, data from liver cancer patients in the International Cancer Genome Consortium (ICGC) were utilized to validate the accuracy of the model. Furthermore, the impact of analgesics on key genes in the prognostic model was assessed using data from the Comparative Toxicogenomics Database (CTD). RESULTS: The study investigated the differential expression of 58 ATs genes in liver cancer compared to normal tissues. Patients were stratified based on ATs expression, revealing varied survival outcomes. Functional enrichment analysis highlighted distinctions in spindle organization, centrosome, and spindle microtubule functions. Prognostic modeling identified low TP53 expression as protective, while elevated CCNA2, NEU1, and HTR2C levels posed risks. Commonly used analgesics, including acetaminophen and others, were found to influence the expression of these genes. These findings provide insights into potential therapeutic strategies for liver cancer and shed light on the molecular mechanisms underlying its progression. CONCLUSIONS: The collective analysis of gene signatures associated with ATs suggests their potential as prognostic predictors in hepatocellular carcinoma patients. These findings not only offer insights into cancer therapy but also provide novel avenues for the development of indications for analgesics.

Advancements in the research of immune checkpoint inhibitors for the treatment of advanced esophageal squamous cell carcinoma.

Esophageal cancer (EC) has a high mortality rate and poor prognosis. Most patients are diagnosed at an advanced stage or with distant metastasis, making surgery impossible. Traditional curative radiotherapy and chemotherapy have limited efficacy. In recent years, with the development of clinical trials, immune checkpoint inhibitors (ICIs) have shown promising results in treating advanced and metastatic esophageal squamous cell carcinoma (ESCC) patients. ICIs have gradually become a primary therapeutic approach for EC. This review summarizes and provides an overview of the current research status and progress of ICIs in the treatment of advanced ESCC patients.

Delayed chylopericardium after radical surgery for esophageal cancer: a case report.

Background: Postoperative chylpericardium is a rare clinical disease that often manifests as chest tightness, shortness of breathdyspnea, and other symptoms of pericardial tamponade. The etiological spectrum of chylopericardium is complex, but the disease is mainly idiopathic. Chylopericardium caused by thoracic surgery is rarely reported, both at home and abroad. Case summary: We report a case of a 65-year-old male patient who developed chylopericardium after thoracoabdominal combined incision and partial esophagogastric anastomosis plus lymph node dissection for 1 month. After pericardiocentesis and drainage, low-fat enteral nutrition, and parenteral nutrition, the patient was cured. Based on this case, this article reviews the literature on the diagnosis and treatment of chylopericardium after thoracic surgery. Conclusion: In conclusion, thoracic surgery (excluding cardiac surgery) can cause delayed chylopericardium. This condition is rarely reported in China, and only a few cases have been reported abroad. Thus, the diagnosis is likely to be missed or misdiagnosed. Early diagnosis and treatment are important to reduce patient discomfort as much as possible.

LncRNA SOX2-OTinhibitionprotects against myocardialischemia/reperfusion-inducedinjury via themicroRNA-186-5p (miR-186-5p)/Yin Yang 1 (YY1)pathway.

Long noncoding RNAs (lncRNAs) exert essential effects in regulating myocardial ischemia/reperfusion (MI/R)-induced injury. This work intended to explore the functions of lncRNA SOX2-OT and its regulatory mechanism within MI/R-induced injury. In this study, gene expression was determined by RT-qPCR. Western blotting was applied for the detection of protein levels. Pro-inflammatory cytokine concentrations, cardiomyocyte viability, and apoptosis were detected via ELISA, CCK-8 and flow cytometry. In the in vitro model, SOX2-OT and YY1 were both upregulated, while miR-186-5p was downregulated. SOX2-OT knockdown attenuated oxygen-glucose deprivation/reoxygenation (OGD/R)-induced cardiomyocyte dysregulation through relieving inflammation, promoting proliferation, and reducing apoptosis in OGD/R-treated H2C9 cells. SOX2-OT positively regulated YY1 expression via miR-186-5p. Moreover, miR-186-5p inhibition or YY1 upregulation abolished the effects of SOX2-OT blocking on the inflammatory responses, proliferation, and apoptosis of OGD/R-challenged H2C9 cells. In conclusion, our results, for the first time, demonstrated that SOX2-OT inhibition attenuated MI/R injury in vitro via regulating the miR-186-5p/YY1 axis, offering potential therapeutic targets for MI/R injury treatment.

Curcumin protects bone biomechanical properties and microarchitecture in type 2 diabetic rats with osteoporosis via the TGFß/Smad2/3 pathway.

Type 2 diabetic osteoporosis (T2DOP) has become a common secondary cause of osteoporosis that accelerates bone loss and leads to bone fractures. The aim of the current study was to investigate the association between the anti-osteoporotic effect of curcumin (Cur) and the transforming growth factor (TGF)ß/Smads signaling pathway. Male Sprague-Dawley rats were used in the experiments. The type 2 diabetes mellitus (T2DM) animals were treated with Cur for 8 weeks and blood lipid markers, bone microstructure and bone biomechanics were then evaluated. The mRNA expression levels of TGFß1, type I TGFß receptor (TßRI), TßRII and Smad2/3 were determined using reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry. The body weight of rats with type 2 diabetes-induced osteoporosis increased (P<0.05), while the lipid (total cholesterol, triglyceride and low-density lipoprotein) and fasting blood glucose levels were decreased by Cur (P<0.05). In addition, Cur significantly improved bone biomechanical properties (maximum load, breaking load, elastic load and the bone rigidity coefficient) and preserved bone microarchitecture (P<0.05). The RT-qPCR and IHC results revealed that Cur increased TGFß1, TßRI, TßRII and Smad2/3 expression levels and promoted Smad2/3 phosphorylation in bones. The present results also indicated that Cur regulated lipid and glucose levels, improved bone biomechanical properties and preserved bone microarchitecture, and that these effects may be mediated via TGFß/Smad2/3 pathway activation.