Rationale:Oseltamivir-induced alimentary tract hemorrhage and liver injury are rarely reported in children and adult individuals. In this study, we described the clinical features and outcomes of oseltamivir-induced alimentary tract hemorrhage and liver injury in a child.Patient concerns:Here, we present a case of a 6-year-old Asian boy with hematemesis and elevated alanine aminotransferase (ALT) (80 U/L) and aspartate aminotransferase (AST) (69 U/L) levels on day 2 of oseltamivir administration. The presence of alimentary tract hemorrhage and liver injury was diagnosed. The ALT level reached 1931.3 U/L, accompanied by an increase in total bilirubin (TBIL) to 53.3 μmol/L on day 15 after oseltamivir administration. Additional tests were performed to determine the presence of viruses that can cause hepatitis and autoantibodies, and the results from these tests were all negative.Diagnosis:Drug-induced liver injury was considered.Interventions:This patient was treated with compound glycyrrhizin and reduced glutathione and glucocorticoid.Outcomes:The liver enzymes recovered within 6 weeks without any symptoms of liver-related diseases after treatment with glucocorticoid. This treatment therefore helps reduce ALT and TBIL levels and protects the liver from further injury.Lessons:Oral oseltamivir is widely used to treat influenza and the adverse effects of this drug were mostly mild. However, clinicians should always be alert for oseltamivir-induced alimentary tract hemorrhage and liver injury when prescribing oseltamivir for children.
BackgroundInnate lymphoid cells (ILCs), so far studied mostly in mouse models, are important tissue-resident innate immune cells that play important roles in the colorectal cancer microenvironment and maintain mucosal tissue homeostasis. Plasmacytoid dendritic cells (pDCs) present complexity in various tumor types and are correlated with poor prognosis. pDCs can promote HIV-1–induced group 3 ILC (ILC3) depletion through the CD95 pathway. However, the role of ILC3s in human colon cancer and their correlation with other immune cells, especially pDCs, remain unclear.MethodsWe characterized ILCs and pDCs in the tumor microenvironment of 58 colon cancer patients by flow cytometry and selected three patients for RNA sequencing.ResultsILC3s were negatively correlated, and pDCs were positively correlated, with cancer pathological stage. There was a negative correlation between the numbers of ILC3s and pDCs in tumor tissues. RNA sequencing confirmed the correlations between ILC3s and pDCs and highlighted the potential function of many ILC- and pDC-associated differentially expressed genes in the regulation of tumor immunity. pDCs can induce apoptosis of ILC3s through the CD95 pathway in the tumor-like microenvironment.ConclusionsOne of the interactions between ILC3s and pDCs is via the CD95 pathway, which may help explain the role of ILC3s in colon cancer.
Wilms tumor (WT) is the most common malignant renal neoplasm in children; however, the underlying molecular mechanisms are not well understood. according to the competing endogenous rna (cerna) theory, long non-coding rnas (lncrnas) can regulate the expression of target genes by adsorbing micrornas (mirnas/mirs). However, the role of lncrnas in WT has not been fully elucidated. The aim of the present study was to construct a cerna network to identify the potential lncRNAs involved in WT. The expression profiles of lncrnas, mirnas and mrnas in 120 WT and six normal tissues were obtained from the Therapeutically applicable research to Generate effective Treatments database. a total of 442 lncRNAs, 214 miRNAs and 4,912 mRNAs were identified as differentially expressed in WT and were enriched in 472 Gene ontology terms (355 biological processes, 89 cellular components and 29 molecular functions) and 18 Kyoto encyclopedia of Genes and Genomes pathways. a lncrna-mirna-mrna cerna network of WT consisting of with 32 lncrnas, 14 mirnas and 158 mrnas was constructed, based on the bioinformatics analysis of the mir target prediction database and the mirnacode, mirTarBase and TargetScan databases. Subsequently, three lncrnas, three mirnas and 17 mrnas, which had a significant effect on the overall survival rate of patients with WT, were identified based on the survival analysis. The three lncrnas were also differentially expressed in the late and early stages of WT and were validated using the GSe66405 dataset obtained from the Gene expression omnibus database. in conclusion, the present study generated a specific lncrna-related cerna network of WT, which may provide a novel perspective on the molecular mechanisms underlying the progression and prognosis of the disease.
Background Ulcerative colitis (UC) is a form of chronic inflammatory bowel disease of nonspecific origin. This study used an RNA-Sequencing (RNA-Seq) approach to evaluate the transcriptomic landscape of a well-stratified treatment-naïve pediatric UC patient population by comparing them with healthy control children. The data were analyzed to evaluate the mechanisms driving UC-related intestinal inflammation and fibrosis. Methods Intestinal mucosal samples from five pediatric UC patients and five healthy controls were analyzed by RNA-Seq, and results were verified by qPCR. A CRISPR/Cas9 approach was used to knock out the expression of HLA-DRB5, and molecular biology techniques were used for additional mechanistic studies. Results In these analyses, 2290 genes were found to be differentially expressed between the UC and control samples, of which 1258 and 1032 were upregulated and downregulated, respectively. Gene Ontology analysis showed that these genes were enriched in extracellular matrix (ECM)-related processes and that 7 of 8 differentially expressed genes of interest (PIK3CD, IL1β, IL1α, TIMP1, MMP1, MMP12, COL6A3, and HLADRB5) were upregulated and involved in ECM-receptor interaction and inflammatory bowel disease-related pathways. Increased HLA-DRB5 expression driven by intestinal bacteria was found to promote IL-1α secretion, leading to intestinal inflammation and fibrosis, suggesting a possible target for the treatment of UC. Conclusion These data suggest that intestinal inflammation is present in pediatric UC patients for extended periods before the onset of symptoms, and intestinal fibrosis begins even during the early stages of UC. Intestinal bacteria were also found to trigger intestinal inflammation and fibrosis, with HLA-DRB5 playing a central role in this process.
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