28 research outputs found
Skin cancer: BCC, SCC, MM and KS (a term of 7 years in Loghman Hakim Hospital)
Skin cancer has a broad and burdensome impact on the health and well-being of Iranian and account for substantial health care costs to the nation. The first most common form of skin cancer is basal cell carcinoma (BCC); followed by the squamous cell carcinoma (SCC) and the incidence of malignant melanoma (MM) is lower but is fatal. Kaposi sarcoma (KS) is a tumor caused by human herpes virus 8. In this study, prevalence and incidence of four skin cancer (BCC, SCC, MM and KS) was investigated by considering to risk factors include age, sex, skin color, sun exposure levels, Lesion location, occupations and timeout to seek treatment. In this study, 95 patients with skin cancers registered in Loghman Hakim hospital during the 7 years from 1998 to 2004 were analyzed. Result depicted that BCC is the most common skin cancer in both sexes and in all types male incidence was significant. Age prevalence of all was about 50 to 80 years. The most common sites of tumor involvement in BCC and SCC were head and neck; KS was lower limb and MM had sporadic lesions. Almost all of patients referred to diagnosis or treatment 1 to 5 years after the initial onset of the disease. Occupations of the majority of patients with skin cancer were farmers. More patients lived in the area with warm and dry climate. In sum up, the skin cancer risk factors are included older ages, residence of warm and dry regions, be male and farmer, and most importantly rate of exposure to sunlight can influence lifestyle of patients that everyone can easily take to protect in different ways.Â
Proteomic Analysis of the Effect of Extremely Low-Frequency Electromagnetic Fields (ELF-EMF) With Different Intensities in SH-SY5Y Neuroblastoma Cell Line
 Introduction: During the last 3 decades, human is exposed to extremely low frequency electromagnetic fields (ELF-EMF) emitted by power lines and electronic devices. It is now well accepted that ELF-EMF are able to produce a variety of biological effects, although the molecular mechanism is unclear and controversial. Investigation of different intensities effects of 50 Hz ELF-EMF on cell morphology and protein expression is the aim of this study.Methods: SH-SY5Y human neuroblastoma cell line was exposed to 0.5 and 1 mT 50 Hz (ELF-EMF) for 3 hours. Proteomics techniques were used to determine the effects of these fields on protein expression. Bioinformatic and statistical analysis of proteomes were performed using Progensis SameSpots software.Results: Our results showed that exposure to ELF-EMF changes cell morphology and induces a dose-dependent decrease in the proliferation rate of the cells. The proteomic studies and bioinformatic analysis indicate that exposure to 50 Hz ELF-EMF leads to alteration of cell protein expression in both dose-dependent and intensity dependent manner, but the later is more pronounced.Conclusion: Our data suggests that increased intensity of ELF-EMF may be associated with more alteration in cell protein expression, as well as effect on cell morphology and proliferation
Proteomic analysis of gene expression during human esophagus cancer
Esophagus cancer is the eighth most common cancer worldwide and particularly high in an area extending from the southern border of the Caspian Sea in Iran across central Asia to China. Since information about this mysterious disease is poor, proteomics may be solving this enigma. Altering gene expression in cancer cell is a remarkable indicator can be detected by proteomics techniques and bioinformatic analysis. In this study, normal and cancerous cells were obtain from patients, total proteins were purified by standard methods, and proteins separated by two dimensional electrophoresis (2DE). Some of proteins were identified by Mass spectrometry (MS-MALDI method). By using bioinformatic analysis illustrate molecular mechanism in this disease. Analysis of gels base on Flicker software and Mass Spectrometry led the same result. 61 protein spots detected in both gels that 21 spots have down regulated and 12 spots have up regulated in cancerous cell than normal. About 14 spots were disappeared in cancer cell while 14 new spots expressed. By using flicker detected 8 Protein that refer to TRFE, SZ07, C1 TC, Kininogen, anexin, keratin, fructosebisphosphate aldolase A and heat shock. Mass spectrometry (MS-MALDI method) identified anexin, keratin, fructosebisphosphate aldolase A and heat shock. Identified proteins were functionally categorized based on Gene Ontology (GO) annotation terms using the DAVID program package. The major molecular functions that annotated with PIR include phosphoprotein, disease mutation while annotated by GO include response to organic substance, response to wounding and cellular homeostasis. The cellular component and molecular function presenting the greatest enrichment that concluded two clusters that the two most importants are cellular homeostasis and extracellular region part. Results reveal that the most of molecular function in cancerous tissue maintenance cellular homeostasis, cell regeneration and repair, so tissues undergo stress try to survive. It can be also concluded that aldolase A, fructose-bisphosphate, keratin 14,  formyltetrahydrofolate synthetase and transferrin can be some diagnostic biomarkers and also drug targets in esophagus cancer.
Proteins expression clustering of Alzheimer disease in rat hippocampus proteome
Because of the huge amounts of proteomic data and demand for new methods of laboratory analysis results, proteins collective analysis, in addition to taking less time, biostatistician assist at identification of new patterns in the data set. In this study, rat hippocampus proteome in normal and Alzheimer's disease (AD) were analyzed by using proteomic techniques and bioinformatics’ analysis. Protein extracts from normal and Alzheimer's rats were separated by using two-dimensional electrophoresis (2DE). The silver staining method was used for detecting spots. Bioinformatics analysis of proteome were performed by progensis same spots software. Bioinformatics and statistical analysis of 2DE gel techniques obtained 760 protein spots were detected in both normal and AD rats. Comparisons between controls and Alzheimer gel containing 20 common proteins were expressed significantly differences. 16 new proteins were expressed in AD, while 36 proteins were suppressed. Proteins clustering by using correlation analysis evaluated 3 clusters in the proteome; Principal component analysis also confirmed the results of clustering. Finally, we can conclude that a significant expression of Alzheimer changes in the hippocampus proteome which are associated with specific biological processes summarized in 3 main clusters indicated 3 principal biological pathways of AD.
Mitochondrial DNA might be influenced in calprotectin-induced cell death
It is generally believed that calprotectin acts via exclusion of extracellular zinc, and/or binding of calprotectin to a cell membrane receptor, and consequently, activation of a signaling pathway for apoptosis. Recently, we suggested that calprotectin may have an “internal target” within cells. Here, using target theory, we provided evidence that this internal target is DNA. Trypan blue (TB) and dimythylthiazol diphenyl tetrazolium bromide (MTT) assays were used to estimate survival of calprotectin-treated cells. TB assay relies on the viability of cell membrane, while MTT assay relies on the functionality of mitochondria. We demonstrated that MTT-based survival values fit to the “single-hit, single-target” model, while TB-based survival values are best matched to the “single-hit, multi-target” model with N=2. Assumption of DNA as the target of calprotectin is fully consistent with the models, since each mitochondrion contains one chromosome and each “cell” is diploid and contains two chromosome sets. To the best of our knowledge this is the first report that suggests mitochondrial DNA is affected during calprotectin-induced cell death. Furthermore, our results explain why toxicity measures (like LD50), when estimated based on TB assay, are sometimes significantly greater than toxicity measures based on MTT assay
A study on Carbon Nanotube-Gene Interaction in Induction of Glial Cells to Neuron Cell
Introduction: Reprogramming different cell to neuron have yet remained attractive field in regenerative medicine, so discovery new methodsor improve existing methods could be helpful. The aim of this study was to evaluate the Carbon Nanotube-Gene Interaction in Induction ofGlial Cells to Neuron Cell.Materials and Methods: Accordingly, we analyzed the transcriptome data of glial and neuron cells to determine thedifferent gene expression in both groups. Then, based on this transcriptome data, the gene chemical interaction was determined to find the mostimportant chemical structure which induces glial cell to neurons. Data extract from transcriptome database related rat cerebral cortex cellsgenerated by RNA sequencing transcriptomic (RNAseq) technique. By comparison neuron against glial cells (astrocyte, oligodenderocyte andmicroglia) determined different gene expression. In Comparative Toxicogenomics Database (CTD) determined the most important chemicalto interact with this gene set. Then by using genetrail2 database determined mechanism of gene set associated to chemicals and miRNA enriched.Results: Result determined different chemical with the risk factor and protective factor properties related to 500 genes that enriched in a neuronin comparison with glial cells. The carbon nanotube is the first important chemicals that interact with 75 genes of 500. Gene ontology analysisdetermined the carbon nanotube effect on genes that induce neurogenesis, neurodevelopment, and differentiation. Genetrail2 release the 29significant miRNAs enriched in gene interacts with carbon nanotube in which miR-34a and miR-449a are the most significant molecules.Network analysis of these genes represents KIT (tyrosine-protein kinase, CD117), Gria1, Syt1, Rab3c, and Tubb3 have central roles inneurogenesis by the carbon nanotube.Conclusion: In sum up, the carbon nanotube is an electrical stimulator that has biocompatibility toinduce glial cell to the neuron which applies as devise lonely or combination with a cell in damage part of the neural tissue
The study of fibroblast proteome changes in the presence of Ethanol
   Ethanol known as ethyl alcohol is being widely used around the world. Many serious diseases are related with its consumption.  Alcohol posses many divers effects on human body including risk of cirrhosis and/or hepatocellular carcinoma. Therefore, analysis of this component is prominent. Fibroblast cells were cultured in various dosages of ethanol. The effective dosage was then investigated by proteomic methods.  Separated proteins of fibroblast cells by Two-Dimensional Gel (2DG) Electrophoresis method based on pI and MW were analyzed based on spots alteration by Same Spot Software. Furthered analysis was carried out with vigorous statistical analysis based on significant folding changes and one-way ANOVA. About 372 protein spots were identified and among them 65 of them were having significant expression profile, which is evaluated as p <0.05. Therefore, ethanol can induce a great impact on protein profile of fibroblast. It is concluded that altering morphologic features and viability, as well as protein expression changes, confirm toxic properties of ethanol in human body.
Study of apoptosis inducing activity of calprotectin on fibroblast cell
One of the prominent types of connective tissue cells is fibroblast that synthesizes and maintains the extracellular matrix of many animal tissues. Previous studies illustrated that calprotectin protein has different cytotoxicity effects on fibroblast cells. Calprotectin is abundant in the neutrophil cytosol; it has growth-inhibitory and apoptosis-inducing activities against various cell types such as tumor cells. The present study tries to introduce mechanism of growth inhibitory effect of calprotectin on human foreskin fibroblast cells (HFFF) and compare to etoposide (chemotherapy agent as control). Calprotectin was purified from human neutrophil by chromatography methods. HFFF cell lines were used, maintained in RPMI 1640 medium supplemented with 10% FCS in a humidified incubator (37 ÂşC & 5% CO2). The HFFF cells were exposed to the different concentrations of calprotectin and etoposide for 24, 48 and 72 hours. Cell proliferation was assessed by using dimethylthiazol diphenyl tetrazolium bromide assay. Flow cytometric analysis was performed to evaluate the cytotoxic mechanism of calprotectin on HFFF cells. Our results revealed that calprotectin and etoposide induce growth inhibition of HFFF in dose- and time-dependent manners. Sensitivity of HFFF cells to cytotoxic effect of human calprotectin was highly remarkable. In addition, growth inhibitory effect of this cytotoxic agent mostly was governed through induction of apoptosis in the HFFF cells. Taken together, calprotectin not only has more potent anticancer activity in comparison with the etoposide, but it also is an apoptosis inducer that acts on the proliferation of normal cells like fibroblasts