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Ascaris lumbricoides is a helminth commonly infecting humans, particularly in developing countries. It causes a range of clinical symptoms; However, many patients are asymptomatic. This article presents a case study of a young man who experienced diffuse abdominal pain and constipation, eventually being diagnosed with partial bowel obstruction due to Ascaris lumbricoides infection. The article emphasizes the importance of considering helminthic infections like ascariasis as a potential cause of intestinal obstruction, especially in endemic areas. Early diagnosis and intervention, including conservative management and anthelminthic drugs, can lead to a full recovery and avoid unnecessary surgery.
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Background: Liver hepatocellular carcinoma (LIHC) is a common cancer with a poor prognosis and high recurrence rate. We aimed to identify potential biomarkers for LIHC by investigating the involvement of hub genes, microRNAs (miRNAs), transcription factors (TFs), and protein kinases (PKs) in its occurrence. Methods: we conducted a bioinformatics analysis using microarray datasets, the TCGA-LIHC dataset, and text mining to identify differentially expressed genes (DEGs) associated with LIHC. They then performed functional enrichment analysis and gene-disease association analysis. The protein-protein interaction network of the genes was established, and hub genes were identified. The expression levels and survival analysis of these hub genes were evaluated, and their association with miRNAs, TFs, and PKs was assessed. Results: The analysis identified 122 common genes involved in LIHC pathogenesis. Ten hub genes were filtered out, including CDK1, CCNB1, CCNB2, CCNA2, ASPM, NCAPG, BIRC5, RRM2, KIF20A, and CENPF. The expression level of all hub genes was confirmed, and high expression levels of all hub genes were correlated with poor overall survival of LIHC patients. Conclusion: Identifying potential biomarkers for LIHC can aid in the design of targeted treatments and improve the survival of LIHC patients. The findings of this study provide a basis for further research in the field of LIHC and contribute to the understanding of its molecular pathogenesis.
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Multiple Myeloma (MM) is a neoplastic hematologic disorder caused by the excessive proliferation of plasma cells and leads to bone lesions, anemia, and kidney failure. No definite etiology has been proposed for MM, but several environmental and genetic risk factors have been implicated so far. Exposure to pesticides, benzene, and organic solvents like methyl chloride have been considered a potential risk factor. Asbestos, ionizing radiation, and wood dust exposure have also been associated with MM. As MM is a relatively rare condition, the number of studies is insufficient, and in many studies, only a few study participants recall exposure to any agents. Therefore, establishing a definite risk factor is cumbersome and further studies with large study samples are needed. By recognizing these occupational risk factors, clinicians can encourage employees to reduce their exposure as more as possible and implement precautionary measures. In this review, we highlighted the current research on the potential association between occupational exposures and MM. Because of these studies, new regulations with the goal of occupational exposure reduction are anticipated in the future.
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Background: Sickle cell disease (SCD) is one of the hematological disorders characterized by a defect in the structure and function of globin chains. Hereditary factors play an important role in the pathogenesis of SCD. We aimed to investigate the genes and pathways related to the pathogenesis of SCD. Methods: Microarray dataset was downloaded from the Gene Expression Omnibus (GEO) database. LIMMA package of R-software was used to detect UP and Down regulations between SCD and control subjects. Enrichment analysis and Protein-protein interaction (PPI) networks were performed using GeneCodis4 software and GeneMANIA database, respectively. PrognoScan database was used to evaluate the relationship between the hub genes and patients' survival. Results: Overall, 447 DEGs were identified in SCD patients compared to control subjects. Out of 447 DEGs, 345 genes were up-regulated and 102 genes were down-regulated. Effective hub genes in SCD pathogenesis include SLC4A1, DTL, EPB42, SNCA, and TOP2A. In addition, hub genes had a high diagnostic value. Conclusion: Evaluation of hub genes in SCD can be used as a diagnostic panel to detect high-risk patients. In addition, by identifying the UP and Down stream pathways, treatment strategies in the monitoring and treatment of patients can be designed.
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Background: Urinary tract infections (UTIs) are a widespread health concern with high recurrence rates and substantial economic impact, and they can increase the prevalence of antibiotic resistance. This study employed an integrated bioinformatics approach to identify key genes associated with UTI development, offering potential targets for interventions. Materials and Methods: For this study, the microarray dataset GSE124917 from the Gene Expression Omnibus (GEO) database was selected and reanalyzed. The differentially expressed genes (DEGs) between UTIs and healthy samples were identified using the LIMMA package in R software. In this section, Enrichr database was utilized to perform functional enrichment analysis of DEGs. Subsequently, the protein-protein interaction (PPI) network of the DEGs was constructed and visualized through Cytoscape, utilizing the STRING online database. The identification of hub genes was performed using Cytoscape's cytoHubba plug-in employing various methods. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic accuracy of hub genes. Results: Among the outcomes of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the tumor necrosis factor (TNF) signaling pathway was identified as one of the notable pathways. The PPI network of the DEGs was successfully established and visualized in Cytoscape with the aid of the STRING online database. Using cytoHubba with different methods, we identified seven hub genes (STAT1, IL6, IFIT1, IFIT3, IFIH1, MX1, and IRF7). Based on the ROC analysis, all hub genes showed high diagnostic value. Conclusion: These findings provide a valuable baseline for future research aimed at unraveling the intricate molecular mechanisms behind UTI.
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Cardiotoxicity is a serious challenge cancer patients face today. Various factors are involved in cardiotoxicity. Circular RNAs (circRNAs) are one of the effective factors in the occurrence and prevention of cardiotoxicity. circRNAs can lead to increased proliferation, apoptosis, and regeneration of cardiomyocytes by regulating the molecular pathways, as well as increasing or decreasing gene expression; some circRNAs have a dual role in cardiomyocyte regeneration or death. Identifying each of the pathways related to these processes can be effective on managing patients and preventing cardiotoxicity. In this study, an overview of the molecular pathways involved in cardiotoxicity by circRNAs and their effects on the downstream factors have been discussed.
Asunto(s)
Antineoplásicos , Cardiopatías , Células Musculares , Neoplasias , ARN Circular , Células Musculares/efectos de los fármacos , Células Musculares/metabolismo , Células Musculares/patología , Neoplasias/tratamiento farmacológico , Neoplasias/genética , Antineoplásicos/efectos adversos , Antineoplásicos/uso terapéutico , Cardiopatías/inducido químicamente , Cardiopatías/genética , Cardiopatías/metabolismo , Apoptosis/efectos de los fármacos , ARN Circular/genética , ARN Circular/metabolismo , HumanosRESUMEN
Various factors are effective in the development of minimal residual disease (MRD), one of which is MicroRNAs (miRNAs). miRNAs and their dysfunction in gene expression have influential role in the pathogenesis of leukemia. Nowadays, treatments that lead to the suppression or replacement of miRNAs have been developed. Focusing on the role of miRNAs in managing the treatment of leukemia, in this review article we have investigated the miRNAs and signaling pathways involved in the process of apoptosis and cell proliferation, as well as miRNAs with oncogenic function in malignant leukemia cells. Among the studied miRNAs, miR-99a, and miR-181a play an essential role in apoptosis, proliferation and oncogenesis via AKT, MAPK, RAS, and mTOR signaling pathways. miR-223 and miR-125a affect apoptosis and oncogenesis via Wnt/B-catenin, PTEN/PI3K, and STAT5/AKT/ERK/Src signaling pathways. miR-100 also affects both apoptosis and oncogenesis; it acts via IGF1 and mTOR signaling pathways.
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Gastrointestinal malignancies are the most prevalent type of cancer around the world. Even though numerous studies have evaluated gastrointestinal malignancies, the actual underlying mechanism is still unknown. These tumors have a poor prognosis and are frequently discovered at an advanced stage. Globally, there is an increase in the incidence and mortality of gastrointestinal malignancies, including those of the stomach, esophagus, colon, liver, and pancreas. Growth factors and cytokines are signaling molecules that are part of the tumor microenvironment and play a significant role in the development and spread of malignancies. IFN-γ induce its effects by activation of intracellular molecular networks. The main pathway involved in IFN-γ signaling is the JAK/STAT pathway, which regulates the transcription of hundreds of genes and mediates various biological responses. IFN-γ receptor is composed of two IFN-γR1 chains and two IFN-γR2 chains. Binding to IFN-γ, causes the intracellular domains of IFN-γR2 to oligomerize and transphosphorylate with IFN-γR1 which activates downstream signaling components: JAK1 and JAK2. These activated JAKs phosphorylate the receptor, creating binding sites for STAT1. STAT1 is then phosphorylated by JAK, resulting in the formation of STAT1 homodimers (gamma activated factors or GAFs) that translocate to the nucleus and regulate gene expression. The balance between positive and negative regulation of this pathway is crucial for immune responses and tumorigenesis. In this paper, we evaluate the dynamic roles of IFN- γ and its receptors in gastrointestinal cancers and present evidence that inhibiting IFN- γ signaling may be an effective treatment strategy.