ABSTRACT
[This retracts the article DOI: 10.7759/cureus.20122.].
ABSTRACT
Recent studies have shown a significant increase in the utilization of computed tomography (CT) scans in the emergency department for a broad spectrum of conditions. This had a significant impact on the identification of patients with serious pathologies in a timely manner. However, the overutilization of computed tomography scans leads to increased identification of incidental findings. For example, pancreatic lesions are not uncommon findings that can be identified in imaging studies performed for other indications. Here, we report the case of a 55-year-old male with a history of urinary stone disease who presented with right flank pain and dysuria. The urinalysis findings revealed numerous red blood cells and leukocytes. Non-contrast computed tomography scan of the abdomen was performed to detect urinary stones, but no hyperdense stones were noted, suggesting the possibility of spontaneous passage of the stone. However, a lesion in the pancreatic tail was observed. This exhibited fat attenuation with no solid component in the pancreatic tail representing a pancreatic lipoma. No surgical intervention was made considering the benign nature of the incidentally detected tumor. Pancreatic lipoma is a very rare benign mesenchymal tumor of the pancreas. Recognition of the classic radiological feature of pancreatic lipoma is essential to avoid unnecessary investigation and procedures.
ABSTRACT
Carbon based nanomaterials, including carbon nanotubes, graphene, nanodiamond and carbon nanoparticles, have emerged as potential candidates for a wide variety of applications because of their unusual electrical, mechanical, thermal and optical properties. However, our understanding of how increased usage of carbon based nanomaterials could lead to harmful effects in humans and other biological systems is inadequate. Our present investigation is focused on the cellular toxicity of carbon nanoparticles (CNPs) on human mesenchymal stem cells (hMSCs). Following exposure to CNPs, cell viability, nuclear morphological changes, apoptosis and cell cycle progression were monitored. Furthermore, the expression of genes involved in both cell death (e.g., P53, TNF3, CDKN1A, TNFRSF1A, TNFSF10, NFKBIA, BCL2L1) and cell cycle regulation (e.g., PCNA, EGR1, E2F1, CCNG1, CCND1, CCNC, CYCD3) were assessed using qPCR. Our results indicated that CNPs reduce cell viability and cause chromatin condensation and DNA fragmentation. Cell cycle analysis indicated that CNPs affect the cell cycle progression. However, the gene expression measurements confirmed that CNPs significantly upregulated the P53, TNF3, CDKNIA, and NFKBIA genes and downregulated the EGR1 gene in hMSCs. Our findings suggest that CNPs reduce cell viability by disrupting the expression of cell death genes in human mesenchymal stem cell (hMSC). The results of this investigation revealed that CNPs exhibited moderate toxicity on hMSCs.
Subject(s)
Carbon/toxicity , I-kappa B Proteins/genetics , Mesenchymal Stem Cells/drug effects , Nanoparticles/toxicity , Tumor Necrosis Factor-alpha/genetics , bcl-X Protein/genetics , Apoptosis/drug effects , Apoptosis/genetics , Carbon/chemistry , Cell Culture Techniques , Cell Cycle/drug effects , Cell Cycle/genetics , Cell Cycle Checkpoints/drug effects , Cell Survival/drug effects , Cell Survival/genetics , Down-Regulation , Gene Expression/drug effects , Humans , NF-KappaB Inhibitor alpha , Nanoparticles/chemistry , Particle Size , Transcriptional Activation/drug effects , Up-RegulationABSTRACT
BACKGROUND: Nigella Sativa (NS) is an herb from the Ranunculaceae family that exhibits numerous medicinal properties and has been used as important constituent of many complementary and alternative medicines (CAMs). The ability of NS to kill cancer cells such as PC3, HeLa and hepatoma cells is well established. However, our understanding of the mode of death caused by NS remains nebulous. The objective of this study was to gain further insight into the mode and mechanism of death caused by NS in breast cancer MCF-7 cells. MATERIALS AND METHODS: Human breast cancer cells (MCF-7) were treated with a methanolic extract of NS, and a dose- and time-dependent study was performed. The IC50 was calculated using a Cell Titer Blue® viability assay assay, and evidence for DNA fragmentation was obtained by fluorescence microscopy TUNEL assay. Gene expression was also profiled for a number of apoptosis-related genes (Caspase-3, -8, -9 and p53 genes) through qPCR. RESULTS: The IC50 of MCF-7 cells was 62.8 µL/mL. When MCF-7 cells were exposed to 50 µL/mL and 100 µL/mL NS for 24 h, 48 h and 72 h, microscopic examination (TUNEL assay) revealed a dose- and time-dependent increase in apoptosis. Similarly, the expression of the Caspase-3, -8, -9 and p53 genes increased significantly according to the dose and time. CONCLUSIONS: NS induced apoptosis in MCF-7 cells through both the p53 and caspase pathways. NS could potentially represent an alternative source of medicine for breast cancer therapy.
Subject(s)
Apoptosis/drug effects , Breast Neoplasms/drug therapy , Nigella sativa/metabolism , Plant Extracts/pharmacology , Tumor Suppressor Protein p53/biosynthesis , Antineoplastic Agents, Phytogenic/pharmacology , Breast Neoplasms/genetics , Caspase 3/biosynthesis , Caspase 3/genetics , Caspase 8/biosynthesis , Caspase 8/genetics , Caspase 9/biosynthesis , Caspase 9/genetics , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , DNA Fragmentation/drug effects , Female , Gene Expression Profiling , Humans , MCF-7 Cells , Seeds/metabolism , Tumor Suppressor Protein p53/geneticsABSTRACT
Dietary phytochemicals have a variety of antitumor properties. In the present study, the antitumor activity of methanolic extract of lemon fruit (lemon extract; LE) (LE) on the MCF-7 breast cancer cell line was investigated in vitro. Apoptotic cell death was analyzed using the TUNEL assay. In addition, the apoptosis mediated by LE extract in the MCF-7 cells was associated with the increased expression of the tumor suppressor p53 and caspase-3. Additionally, the expression of a pro-apoptotic gene, bax, was increased, and the expression of an anti-apoptotic gene, bcl-2, was decreased by LE extract treatment, resulting in a shift in the Bax:Bcl-2 ratio to one that favored apoptosis. The expression of a major apoptotic gene, caspase-3, was increased by LE extract treatment. In light of the above results, we concluded that LE extract can induce the apoptosis of MCF-7 breast cancer cells via Bax-related caspase-3 activation. This study provides experimental data that are relevant to the possible future clinical use of LE to treat breast cancer.