RESUMO
Background: Patients undergoing chemotherapy often encounter troubling and common side effects, notably Chemotherapy-induced nausea and vomiting (CINV). This side effect not only impairs the patient's quality of life but could also result in the interruption or discontinuation of the chemotherapy treatment. Consequently, research into CINV has consistently remained a focal point in the realm of clinical medicine. In this research domain, bibliometric analysis has not been conducted. The purpose of this study is to deliver a thorough summary of the knowledge framework and key areas of interest in the field of Chemotherapy-induced nausea and vomiting, using bibliometric methods. This approach aims to furnish novel concepts and pathways for investigators working in this area. Methods: Publications focusing on Chemotherapy-induced nausea and vomiting, spanning from 2004 to 2023, were identified using the Web of Science Core Collection (WoSCC) database. Tools such as VOSviewer, CiteSpace, and the R package "bibliometrix" were employed for this bibliometric analysis. Results: This research covers 734 publications from 61 countries, with the United States and China being the primary contributors. There has been a significant rise in the volume of papers published in the most recent decade compared to the one before it, spanning over the past twenty years. However, the annual publication rate in the last ten years has not shown a significant upward trend. The University of Toronto, Merck & Co., Sun Yat-sen University, and Helsinn Healthcare SA emerged as the principal research institutions in this field. Supportive Care in Cancer stands out as the most frequently published and cited journal in this domain. These works are contributed by 3,917 authors, with Rudolph M Navari, Matti Aapro, Shimokawa Mototsugu, and Lee Schwartzberg being among those who have published the most. Paul J. Hesketh is notably the most co-cited author. The primary focus of this research field lies in exploring the mechanisms of CINV and the therapeutic strategies for managing it. Key emerging research hotspots are represented by terms such as "Chemotherapy-induced nausea and vomiting," "nausea," "vomiting," "chemotherapy," and "antiemetics." Conclusion: This represents the inaugural bibliometric study to thoroughly outline the research trends and advancements in the field of CINV. It highlights the latest research frontiers and trending directions, offering valuable insights for scholars engaged in studying CINV.
RESUMO
Hepatitis B virus (HBV), a common blood transmission pathogen worldwide, can lead to viral hepatitis, cirrhosis, liver cancer, and other liver diseases. In particular, occult hepatitis B virus infection (OBI) may be caused by an immune response leading to suppressed virus replication. Gut microbiota can change the immunity status of the human body and, therefore, affect the replication of HBV. Thus, to identify whether there are differences in gut microbiota between HBV carriers and OBI carriers, we collected fecal samples from 18 HBV carriers, 24 OBI blood donors, and also 20 healthy blood donors as negative control. After 16S sequencing, we found that the abundance of Faecalibacterium was significantly reduced in samples from OBI blood donors compared with those from healthy blood donors. Compared with samples from HBV carriers, the samples from OBI blood donors had a significantly increased abundance of Subdoligranulum, which might stimulate immune activation, thus inhibiting HBV replication and contributing to the formation of occult infection. Our findings revealed the potential role of gut microbiota in the formation of OBI and further provided a novel strategy for the treatment of HBV infection.IMPORTANCEOccult hepatitis B virus infection (OBI) is a special form of hepatitis B virus infection with hepatitis B surface antigen (HBsAg) positive and hepatitis B virus (HBV) DNA negative. Gut microbiota may contribute to the immune response leading to suppressed virus replication and, thus, participates in the development of OBI. The study on gut microbiota of OBI blood donors provides novel data considerably advancing our understanding of the immune mechanism for the determination of occult hepatitis B virus infection, which is helpful for improving the strategy of the treatment of HBV infection.
Assuntos
Fezes , Microbioma Gastrointestinal , Vírus da Hepatite B , Hepatite B , Humanos , Vírus da Hepatite B/genética , Vírus da Hepatite B/fisiologia , Masculino , Hepatite B/virologia , Hepatite B/microbiologia , Hepatite B/imunologia , Adulto , Feminino , Fezes/microbiologia , Fezes/virologia , Pessoa de Meia-Idade , Portador Sadio/microbiologia , Portador Sadio/virologia , DNA Viral/genética , Replicação Viral , Antígenos de Superfície da Hepatite B/sangue , RNA Ribossômico 16S/genética , Adulto Jovem , Doadores de Sangue , Bactérias/classificação , Bactérias/isolamento & purificação , Bactérias/genéticaRESUMO
OBJECTIVE: To explore potential pathogenic processes and possible treatments using unbiased and reliable bioinformatic tools. METHODS: Gene expression profiles of control and hepatocyte growth factor (HGF) samples were downloaded from CNP0000995. Analysis of differentially expressed genes (DEGs) was conducted using R software (version 4.2.1, R Foundation, Vienna, Austria). Functional enrichment analyses were performed using the Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) databases, then the proteinprotein interaction (PPI) network was constructed to screen the top 10 hub genes. Finally, five genes related to cell junctions were selected to build gene-miRNA interactions and predict small-molecule drugs. RESULTS: A total of 342 downregulated genes and 188 upregulated genes were detected. Candidate pathways include the extracellular matrix (ECM) receptor interaction pathway, the TGF-ß signalling pathway and the cell adhesion molecule (CAM) pathway, which were discovered through KEGG and GSEA enrichment studies. GO analyses revealed that these DEGs were significantly enriched in cell adhesion, the adherens junction and focal adhesion. Five hub genes (CDH1, SNAP25, RAC2, APOE and ITGB4) associated with cell adhesion were identified through PPI analysis. Finally, the gene-miRNA regulatory network identified three target miRNAs: hsa-miR-7110-5p, hsa-miR-149-3p and hsa-miR-1207-5p. Based on the gene expression profile, the small-molecule drugs zebularine, ecuronium and prostratin were selected for their demonstrated binding activity when docked with the mentioned molecules. CONCLUSION: This study offered some novel insights into molecular pathways and identified five hub genes associated with cell adhesion. Based on these hub genes, three potential therapeutic miRNAs and small-molecule drugs were predicted, which are expected to provide guidance for the treatment of patients with HGF.
Assuntos
Fibromatose Gengival , MicroRNAs , Humanos , MicroRNAs/genética , Adesão Celular , Adesões FocaisRESUMO
Hepatitis B virus (HBV) genotype C is a prevalent HBV genotype in the Chinese population. Although genotype C shows higher sequence heterogeneity and more severe liver disease than other genotypes, its pathogenesis and immunological traits are not yet fully elucidated. In this study, we first established and chemically synthesized the consensus sequence based on representative 138 full-length HBV genotype C genomes from the Chinese population. The pHBV1.3C plasmid system, containing a 1.3-fold full-length HBV genotype C consensus sequence, was constructed for subsequent validation. Next, we performed functional assays to investigate the replicative competence of pHBV1.3C in vitro through the transient transfection of HepG2 and Huh7 cells and validated the in vivo function via a hydrodynamic injection to BALB/c recipient mice. The in vitro investigation revealed that the extracellular HBV DNA and intracellular replicative intermediate (i.e., pregenomic RNA, pgRNA) were apparently measurable at 48 h, and the HBsAg and HBcAg were still positive in hepatoma cells at 96 h. We also found that HBsAg and HBeAg accumulated at the extracellular and intracellular levels in a time-dependent manner. The in vivo validation demonstrated that pHBV1.3C plasmids induced HBV viremia, triggered morphological changes and HBsAg- or HBcAg- positivity of hepatocytes, and ultimately caused inflammatory infiltration and focal or piecemeal necrosis in the livers of the murine recipients. HBV protein (HBsAg) colocalized with CD8+ T cells or CD4+ T cells in the liver. F4/80+ Kupffer cells were abundantly recruited around the altered murine hepatocytes. Taken together, our results indicate that the synthetic consensus sequence of HBV genotype C is replication-competent in vitro and in vivo. This genotype C consensus genome supports the full HBV life cycle, which is conducive to studying its pathogenesis and immune response, screening novel antiviral agents, and further optimizing testing and therapeutics.