نگار دیناروند

Epstein-Barr virus (EBV), human herpesvirus 8 (HHV-8), hepatitis B virus (HBV), human papilloma virus (HPV), Merkel cell polyomavirus (MCPyV), human lymphotropic virus type 1 (HTLV-1) and Hepatitis C virus (HCV) are among the most important viruses that cause cancer in humans. These viruses are collectively known as oncoviruses due to their potential to induce malignant transformations in host cells. Oncoviruses exert their cancer-causing effects by utilizing various viral oncoproteins and non-coding RNAs, which can drive host cells toward malignancy through multiple pathways. One critical strategy these viruses employ involves altering the host cell's regulatory mechanisms, particularly by influencing DNA methylation processes.DNA methylation is a crucial modification that occurs on the promoter regions of genes, effectively reducing their expression levels. Under normal cellular conditions, a delicate balance of methylation and demethylation is maintained by a specific set of enzymes. Key players in this process include DNA methyltransferases (DNMTs) and TET methylcytosine dioxygenases (TETs), which are pivotal in regulating gene expression through methylation. These enzymes are prime targets for oncoviruses because, by altering their activity, viruses can hijack the host cell's regulatory machinery. Viral oncoproteins, though diverse in structure and function, often converge on disrupting the expression of these enzymes. By doing so, they induce widespread changes in DNA methylation patterns, effectively reprogramming the gene expression landscape of the host cell. This reprogramming is not random; rather, it is a calculated mechanism through which oncoviruses can manipulate the cell cycle, promoting uncontrolled cellular proliferation and progression towards cancer. By suppressing or activating specific genes, these viruses can push cells past normal checkpoints, eventually leading to tumor formation. Despite the critical role of DNA methylation in cancer development, the precise mechanisms by which oncoviruses modulate these methylation processes are not fully understood. Researchers have made significant progress in exploring the connection between viral infections and cancer, but many of the detailed pathways through which oncoviruses control methylation remain to be elucidated. As a result, this area remains a fertile ground for further research, offering potential avenues for therapeutic intervention in virus-induced cancers.

Readmission of patients refers to the return of a patient to the hospital after initial discharge, recognized as an indicator of hospital service quality. An increased readmission rate generally suggests a deficiency in care quality or incomplete treatment, potentially leading to increased costs and socioeconomic issues. This study aims to evaluate the impact of care interventions on reducing patient readmissions at Abuzar Children’s Hospital in Ahvaz.

This descriptive study was conducted at Abuzar Children’s Hospital in Ahvaz from April 2021 to October 2023. Inclusion criteria consisted of discharge and subsequent readmission. Care interventions aimed at reducing readmission rates were implemented from October 2022 to October 2023, with data collected from patient records.

In 2021 and 2022, readmission rates were 0.41% and 0.42%, respectively, with the most common causes being disease relapse and discharge against medical advice. The highest readmission rates were in the neonatal (25.3%) and general (21.1%) departments. Following the interventions, there was a significant decrease (33.33%) in readmissions during the first half of 2023 compared to 2021 and 2022. Additionally, post-surgical infections and cases of discharge against medical advice were reduced.

Understanding the factors leading to readmission can help improve healthcare service quality and reduce costs. The findings indicate that regular care interventions can effectively decrease hospital readmission rates and enhance the quality of healthcare services. It is recommended that health-care interventions be tailored to specific age groups for more effective reduction in readmission rates.

Skin cancer is one of the most common types of cancer worldwide. In addition to ultraviolet radiation which is a well-known contributing factor, other potential factors have recently been proposed that may contribute to the development of skin cancer. Therefore, the aim of this study is the investigating the role of skin microbiota factors, trace elements and genetic factors in the risk of skin cancer. Scientific articles available in PubMed، Google Scholar, and Web of Science (WOS) databases were utilized for this study. Various studies have shown that microbial dysbiosis in human microbiota is one of the effective factors in the development and treatment of skin cancer. Additionally, research has explored the association between skin cancer and exposure to trace elements such as arsenic, cadmium, chromium, copper, iron, selenium, and zinc. While some studies indicate that exposure to arsenic is associated with an increased risk of keratinocyte cancer, contradictory results have been reported regarding the role of other elements. Furthermore, some diseases and genetic disorders such as basal cell carcinoma and malignant melanoma predispose individuals to skin cancers. Given the substantial prevalence of skin cancer and the paucity of existing research, further investigations into risk factors and preventive measures are imperative.