The newest class of noncoding RNAs with distinctive characteristics is called circular RNAs (circRNAs). These novel RNAs are more stable than other RNAs because they lack 5’ and 3’ ends, instead having their two ends created from pre-mRNA through a process called back-splicing. They are also widely expressed in a variety of species, including viruses, plants, and mammals. There is growing evidence that circRNAs are enriched in the NF-κB pathway. The development of many types of malignancies is associated with aberrant activation of the NF-κB pathway. Recent findings indicate that the circRNA/NF-κB axis controls the expression of genes linked to cancer and, consequently, the growth of tumors. Moreover, circRNAs might interact with the NF-κB pathway to affect biological processes of cells. A comprehensive understanding of the molecular processes behind the involvement of circRNA linked to the NF-κB pathway in the progression of distinct malignancies would provide novel opportunities for cancer therapy. Therefore, this article will briefly discuss the function of circRNAs and the NF-κB pathway in cancer. Next, it will address the crucial role that circRNAs associated with NF-κB play in the progression of different types of malignancies.

Objectives: Type 2 diabetes has become a global health burden, especially in developing nations, and is frequently linked to dyslipidemia. While various medications are available, there is a growing interest in herbal remedies such as Nigella sativa (N. sativa) as alternative treatments for type 2 diabetes. In this systematic review and meta-analysis, the objective was to assess the impact of N. sativa on the lipid profile of patients with type 2 diabetes.
Methods: Online databases, including Web of Science, Scopus, PubMed, and EMBASE, were searched. Changes in lipid profile parameters were reported as weighted mean differences, along with a 95% confidence interval. Sensitivity analysis, quality assessment, subgroup analysis, and publication bias were evaluated in the eligible studies.
Results: The study was performed on eight randomized controlled trials (RCTs) involving 1030 participants. According to the findings, supplementation of N. sativa in the form of seed powder or oil significantly reduced total cholesterol and LDL-cholesterol levels, while increasing HDL-cholesterol levels in patients with type 2 diabetes. The funnel plot exhibited visual symmetry for the studies included in the meta-analysis.
Conclusion: The findings indicate that N sativa may be beneficial as an adjunctive treatment alongside standard medications for managing dyslipidemia in individuals with type 2 diabetes.

Objectives: The aim of this study is to evaluate the potential effect of caffeic acid (CAF) on the growth of breast cancer cells, in addition to determining the contributing role of caspases, mitochondria, and oxidative status.
Methods: MCF-7 and MDA-MB-468 breast cancer cells were exposed to varying concentrations of CAF for different periods of time. The potential cytotoxic effect was measured using the MTT assay. The activities of caspase 3 and caspase 8, as well as the cellular level of reactive oxygen species (ROS) and the level of mitochondrial membrane potential (Δψm), were evaluated in different groups of cells.
Results: The findings showed that CAF decreased the percentage of MCF-7 and MDAMB-468 cells in a manner that depended on the dose and duration of exposure. The death of breast cancer cells induced by CAF was associated with an increase in ROS level in both cell lines. The decrease in mitochondrial membrane potential (Δψm) following CAF treatment suggests that mitochondrial dysfunction may be involved in the death of breast cancer cells induced by CAF. Importantly, the activity of caspase 8 increased after treatment, indicating the potential involvement of the extrinsic apoptosis pathway in the
inhibition of breast cancer cell growth by CAF. The dosage of 20μm of CAF following 48 hours of incubation appeared to have the most significant impact on breast cancer cells.
Conclusion: The study highlights the potential pro-apoptotic effect of CAF in both estrogen-positive and estrogen-negative breast cancer cells. This, in conjunction with other evidence, may lead to new insights for more effective therapeutic approaches in breast cancer.

Objectives: Advanced glycation end products (AGEs) play an important role in the development and progression of diabetic complications. The receptor for AGE (RAGE) is the ligand-binding site of AGE that initiates and accelerates the atherosclerotic process. Plasminogen activator inhibitor-1 (PAI-1) is a prothrombotic factor that has been proposed as a biological marker for prognostic assessment, monitoring of microvascular and macrovascular complications in diabetes. The purpose of this study is to investigate the effects of aminoguanidine on RAGE and PAI-1 expression levels in the liver of streptozotocin-induced diabetic rats.
Methods: Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ, 50 mg/kg). On day 3, diabetic rats were administered 50, 100, and 200 mg/kg/day of aminoguanidine. The expression of PAI-1 and RAGE in the liver tissue was evaluated using real-time PCR.
Results: PAI-1 and RAGE gene expression levels were higher in the liver of the diabetic rats compared to the control group. Aminoguanidine at 50, 100, and 200 mg/kg decreased PAI-1 and RAGE gene expression in the liver (p<0.001 at all doses). However, these genes were downregulated only at a dose of 200 mg/kg in healthy rats (p<0.0001). In addition, hepatic AGE protein levels were significantly decreased following treatment of the diabetic rats with aminoguanidine (p<0.001). There was also a significant correlation between AGE protein concentration and the expression of PAI-1 and RAGE.
Conclusion: In summary, the data of the present study suggest that aminoguanidine reduced the expression of PAI-1 and RAGE in the liver of the diabetic rats.

Objectives: Thyroid Ultrasonography (US) is recommended as a valuable tool for evaluating the status and function of the thyroid gland. The objective of this study was to compare and analyze the thyroid ultrasonography outcomes in children and adolescents who have normal thyroid function and thyroid antibodies.
Methods: A cross-sectional study was conducted on a group of 233 selected females aged 9 to 14 years old. Blood samples were obtained from the subjects and analyzed for thyroid hormones and thyroid autoantibodies. Additionally, a thyroid ultrasound was performed to provide an in-depth evaluation.
Results: Of all the participants, 25% displayed hypoechogenicity. Individuals with reduced echogenicity had higher median levels of thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (TPO-Ab), and thyroglobulin antibody (Tg-Ab) compared to those with normal echogenicity. Moreover, those with hypoechogenicity had significantly higher thyroid volume (TVol), iodine status, and thyroglobulin levels than their counterparts with normal echogenicity. Hypoechogenicity was also significantly associated with higher levels of TPO-Ab, Tg-Ab, and TSH. Logistic regression analysis revealed that high TSH and TPO-Ab levels were associated with a higher risk of irregular echo patterns and thyroid autoantibodies.
Conclusion: The results revealed that irregular thyroid patterns in the ultrasonography were useful for assessing thyroid structure and dysfunction. Moreover, elevated TPOAb, Tg-Ab, and TSH concentrations in the serum may indicate thyroid malfunction. Ultrasound can help to identify early thyroid dysfunction along with the standard thyroid assessment biomarkers.

Objectives: The proprotein convertase subtilisin/kexin type 7 (PCSK7) enzyme is encoded by the PCSK7 gene and is involved in the processing and activation of latent precursor proteins. Previous studies have reported that some PCSK7 variants are associated with markers of body iron stores and lipid profiles, as well as obesity and insulin resistance. The aim of this study was to investigate the association of the rs236918 variant of PCSK7 with metabolic syndrome (MetS) and its related components.
Methods: In this cross-sectional study, 325 participants in the age group of 25 to 86 years were examined. Standard protocols were employed to measure body mass index, blood pressure, fasting blood glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Individuals with metabolic syndrome (MetS) were identified in accordance with the guidelines set by the National Cholesterol Education Program. Genotype was determined using the PCR-RFLP method.
Results: The findings revealed that there was no association between the rs236918 variant and increased risk of MetS or its components and also plasma lipid profile.
Conclusion: Overall, the findings exhibit no significant association between the PCSK7 rs236918 polymorphism and MetS in this population. Although these results may be due to sample size and power issues, the role of lifestyle factors and other genes in the development of MetS appears to be more important in this population. Therefore, further research is required to validate these results.

Objectives: An abnormal buildup of Quinolinic Acid (QuA) is usually linked to the death of nerve cells and a condition known as neuritis in various forms of neurodegenerative illness. Alpha Lipoic Acid (ALA) has substantial antioxidant properties, according to previous studies. However, the protective effects of ALA against the neurotoxicity induced by QuA are unknown. This work aimed to determine whether ALA could shield the SH-SY5Y neuroblastoma cell line from QuA induced neurotoxicity.
Methods: Cell viability was assessed using the MTT assay, while cell cycle and apoptotic effects were evaluated using flow cytometry. Cellular levels of reactive oxygen species (ROS) were also examined.
Results: The findings showed that ALA, at non-toxic concentrations, had a protective effect against QuA-induced toxicity. Moreover, pretreatment with ALA reduced the number of cells that underwent apoptosis. Also, it was found that the percentage of apoptotic cells (i.e., those in the sub-G1 phase) was considerably increased following QuA therapy. ALA also dramatically reduced the production of ROS by QuA.
Conclusion: The results suggest that ALA appears to be an effective neuroprotectant and antioxidant against QuA-induced neurotoxicity.