فهرست مطالب mehrnoosh shanaki

 To investigate the association of adipose tissue transcript levels of IL-1β, IL-6, TNF-α, and MCP-1 with various adiposity indices in obese women.

 Real-time PCR was carry out to investigate the mRNA expression level of the mentioned genes in VAT and SAT from all participants.

 The results presented higher mRNA levels of IL-6 and MCP-1 in SAT and VAT of obese women, compared to normal-weight women. As well, results showed a positive correlation of IL-6 and MCP-1 with HOMA-IR. Obesity indices including BMI, hip, and WHtR were considerably higher in the obese group in comparison with the control group. More importantly, we observed a positive correlation of mRNA expression of these pro-inflammatory factors in adipose tissues with some obesity indices.

 We have shown here that adipose tissue transcript levels of pro-inflammatory cytokines were significantly higher in obese participate than non-obese participants. In obese individuals, this proinflammatory molecules was significantly correlated with various obesity indices. These results suggest that targeting obesity and adipose tissue could prevent the high expression of cytokine.

Genome-wide association studies (GWAS) have been the primary tool for an unbiased study of the genetic background of coronary artery disease (CAD). They have identified a list of single-nucleotide polymorphisms (SNPs) associated with coronary artery disease (CAD). In this study, we aimed to replicate the association of rs2954029 and rs6982502, a GWAS identified SNP, to CAD in an Iranian population.

A sample of 285 subjects undergoing coronary angiography, including 134 CAD patients and 151 healthy. The genotype determination of rs2954029 and rs6982502 SNPs performed using the high-resolution melting analysis (HRM) technique. 

Our results revealed that the TT genotype of rs2954029 (p= 0.009) and rs6982502 (p< 0.001) were significantly higher in CAD patients compared with controls. Binary logistic regression showed that rs6982502 and rs2954029 increase the risk of CAD incidence (2.470 times, p= 0.011, 95% CI= [1.219-4.751], and 2.174 times, p= 0.033, 95% CI= [1.066-4.433] respectively). After adjusting for confounders, we found that rs6982502 and rs2954029 are significantly associated with CAD risk.

These data showed that the TT genotype of rs2954029 and rs6982502 is associated with the risk of CAD in a hospital-based sample of the Iranian population, which has replicated the result of recent GWAS studies.

An unbounded number of events exist beneath the intricacy of each particular hematologic malignancy, prompting the tumor cells into an unrestrained proliferation and invasion. Aberrant expression of cyclin-dependent kinases (CDKs) is one of these events which disrupts regulation of cell cycle and subsequently, results in cancer progression. In this study, we surveyed the repressive impact of multi-CDK inhibitor AT7519 on a panel of leukemia-derived cell lines. Our data underlined that AT7519 abated the survival of all tested cells; however, in an overview, the response rate of leukemic cells to the inhibitor was varied irrespective of p53 status. Notably, the less sensitivity of leukemia cells to AT7519 was found to be mediated partly by the compensatory activation of c-Myc oncogene which was confirmed by the induction of a superior cytotoxicity upon its suppression in less sensitive cell. The blockage of cell cycle, as announced by induction of sub-G1 arrest as well as reduced S phase, resulted in a significant decrease in survival of acute promyelocytic leukemia (APL)-derived NB4 cells, as the most sensitive cell line, either as monotherapy or in combination with arsenic trioxide. Anti-leukemic effects of the inhibitor were further verified by apoptosis analysis, where we discovered that AT7519 induced apoptosis via alteration of pro- and anti-apoptotic genes in NB4. All in all, this study proposed that AT7519 is a rewarding agent opposed to APL; however, additional examinations should be performed to determine the advantages of this inhibitor in clinical setting.

Obesity, a medical condition with impaired adipokine secretion and function, has a detrimental effect on insulin and glucose metabolism. CTRP3 and CTRP9 are adipokines with possible roles in energy homeostasis regulation. We sought to compare CTRP3, CTRP9, and inflammatory gene expression in subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) from obese women who underwent bariatric surgery and non-obese women as controls.

For this study, the investigators recruited 20 morbidly obese women (BMI> 35) who qualified for bariatric surgery and 20 normal-weight women (BMI< 25) who underwent elective surgeries. Real-time PCR was performed to investigate mRNA expression of CTRP3, CTRP9, and the inflammatory genes IL1-β, IL-6, MCP-1, and TNF-α in SAT and VAT from both obese patients and controls.

We observed that CTRP3 mRNA levels were significantly greater in VAT from obese patients than from controls (P< 0.0003). Also, patient group had higher levels of CTRP9 that control group (P< 0.0026). Inflammatory cytokines were markedly increased in SAT of obese patients compared to controls (P< 0.05). In addition, our results revealed a positive correlation of CTRP9 with HOMA-IR and waist circumference in VAT and CTRP3 with IL-1β, MCP-1, and TNF-α in SAT.

Both CTRP3 and CTRP9 expression were significantly higher in VAT from obese patients than from controls, and CTRP3 expression positively correlated with inflammatory parameters. Our findings indicate that CTRP3 and CTRP9 might be important in regulating glucose metabolism and obesity-related conditions such as inflammation.

Nonalcoholic fatty liver diseases (NAFLD) is one of the main chronic liver diseases and raises the risk of morbidity and mortality due to its inevitable outcomes. Understanding the clinical manifestations of the liver is critical to identify NAFLD patients with the greatest risk of developing nonalcoholic steatohepatitis and cirrhosis. In the liver, C1q/TNF-related protein 1 (CTRP1) modulates both glucose and lipid metabolism and improves insulin sensitivity which may affect the pathologies of the liver. 

This study was conducted on 22 patients with NAFLD confirmed by ultrasonography and 21 healthy subjects. Clinical and histological variables were analyzed. The ultrasonography procedure was used to quantity Common bile duct (CBD). Liver stiffness (LS) was measured by transient elastography.

There was a significant difference in CTRP1 levels between NAFLD patients and controls (p=0.032). Moreover, there was a significant positive correlation between CTRP1 level and liver enzymes including AST (r=0.667; p=0.001), ALT (r=0.433; p=0.044), and γ-GT (r=0.428; p=0.047) in NAFLD patients. There was also a significant positive correlation between CTRP1 level and CBD (r= 0.469; p=0.028) in NAFLD patients. Moreover, the largest CBD was measured as 5.99 mm.

It seems that CTRP1 is a novel adipokine related to the pathogenesis of NAFLD and is associated with the clinical manifestations of the liver such as liver enzymes, and CBD.

The vascular endothelial growth factor (VEGF), as an angiogenic cytokine, binds endothelial cell receptors and stimulates angiogenesis and collateral formation. We evaluated the association between VEGF plasma levels and the gene polymorphism rs699947 and the formation of coronary collaterals in patients with coronary artery disease. A total of 195 patients with ≥70% narrowing in at least 1 coronary vessel (according to coronary angiography) were included in the study. The presence of the rs699947 polymorphism within the promoter of the VEGF gene was investigated using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The plasma VEGF concentration was quantified via the ELISA method. The Rentrop method was used to grade the extent of collateral development. There was no significant difference in VEGF levels between the groups with good and poor collaterals. The frequency of the A allele of rs699947 was found to be higher in the patients with good collaterals than in those with poor collaterals (P=0.014). The odds ratio of good collaterals for AA was 2.67 (P=0.025) when compared with the CC genotype. Further, our additive model revealed an association between the rs699947 polymorphism and collateral formation (OR: 1.96, 95% CI: 1.05–3.65, P=0.033). The rs699947 polymorphism might be a novel genetic factor affecting collateral development in Iranian patients with coronary artery disease.

Proteinuria is one of the symptoms that affects the functioning of the kidneys and 24-hour urine protein measurement is one of the key methods for diagnosis of renal failure and urinary tract infection. Investigating the relationship between the results of various methods of measuring 24-hour urine protein can increase the efficiency of proteinuria detection using these methods. Turboidometric-based methods such as trichloroacetic acid (TCA) and benzethonium chloride (BEC) are among the methods used to measure urine protein. The aim of this study was to evaluate the correlation between urine protein measurements with TCA in comparison with BEC. This study was performed on 116 patients referring to Massoud medical diagnostic laboratory in Tehran. The 24-hour urine sample were taken. Then, the amount of urine protein was measured by both TCA and BEC method at 495 and 512 nm wavelengths respectively. The results obtained using Pearson correlation test showed that the correlation coefficient for both TCA and BEC methods is 0.914 (Pvalue <0.001).  Passing and Bablok regression analysis showed that the average protein concentration of the urine with BEC method was 17.31 ± 19.81 and for the TCA method   was 17.40 ± 20.59 mg / dl. In this study, it was shown that there is no difference between the measured results in the range of 1-150 mg/dl of 24-hour urine protein with both TCA and BEC method. Also, there was a good agreement in correlation between the results of both TCA and BEC in the range of 1-150mg, and in general, the data from the two methods were in agreement with each other.

Oxidative stress has been shown to be the most significant influential factor in cancer pathogenesis. Follicular cells are affected in papillary thyroid carcinoma (PTC), which is the most prevalent thyroid cancer associated with oxidative stress. As a noninvasive source of body metabolism, saliva has recently attracted the attention of researchers as an investigative specimen. The present study aimed to evaluate and compare the levels of total antioxidant capacity (TAC) and malondialdehyde (MDA) in the blood and saliva samples of PTC patients and healthy control subjects.
This case-control study was conducted on the patients with PTC referring to Taleghani Hospital in Tehran, Iran. Age- and gender-matched healthy volunteers were selected as the control group. Blood and saliva samples were obtained from all the subjects. Measurement of the MDA and TAC levels was performed using a commercial kit (ZellBio GmbH, Germany) based on colorimetric methods. Data analysis was performed in MedCalc software version 14.8.1.
In total, 33 PTC patients and 33 healthy subjects were enrolled in the study with the mean age of 34.6 ± 8.02 years. No statistically significant differences were observed in the demographic characteristics of the participants. Serum TAC and MDA levels were significantly lower and higher in the PTC group (P According to the results, PTC patients had oxidant/antioxidant imbalance, which could increase the risk of PTC. Furthermore, there were no significant differences in the TAC and MDA levels measured in the saliva of the PTC patients and control subjects. This finding could be attributed to the ultrafiltration in plasma, which involves the seeping-through of the plasma molecules, not allowing the use of saliva as a substitute for serum or plasma.

Tumor angiogenesis is an important procedure for the tumor development as it confirms oxygen and nutrients source to increase cells through the expansion of new blood vessels, potentially causing cancer development and metastasis. Emodin, a tyrosine kinase inhibitor, is an innate anthraquinone derivative found in the roots and rhizomes of several plants. Pharmacological studies have revealed that emodin displays various biological roles, such as anti-inflammatory, antibacterial and anticancer action. Studies have confirmed that emodin prevents cell growth in some types of cancer cells. Therefore, inhibition of angiogenesis is a new strategy for cancer treatment.
In this study, we aimed to determine the effect of emodin on expression of VEGF-A and VEGFR-2 genes in MCF-7 cell line.
Comparative cell viability was measured by MTT assay after treatment with different concentrations of emodin (0, 10, 20, 30, 40 and 50μM) for 24, 48, 72 hours. To investigate apoptosis in cells treated with emodin (0, 10, 20, 30, 40 and 50 µM), flow cytometry was used. Finally, alterations in expression of VEGF-A and VEGFR-2genes were analyzed by real time PCR.
Emodin showed an anti-cancer effect with concentration of 20 μM as IC50 in MCF-7 cells. Emodin induced apoptosis and significantly reduced mRNA level of VEGF-A and VEGFR-2 gene in MCF-7 cell line in a dose dependent manner.
Based on results obtained, emodin significantly reduced mRNA level of VEGF-A and VEGFR-2 gene in MCF-7 cell line in a dose dependent manner.

The poor prognosis of breast cancer is due to its resistance to the conventional treatments. Therefore, researchers are studying about herbs which have anticancer effects. Emodin is a hydroxy-anthraquinone that is found in many medicinal plants and has biological and anticancer effects. According to previous studies, it inhibited the growth of cancer cells by apoptosis.
In this study, we aimed to determine the effect(s) of emodin on growth and proliferation of SKBR3 cancer cells.
SKBR3 cells were cultivated for 24 hours. Then different concentrations of emodin (0, 10, 25 and 50 µM) were added to the test wells and incubated for 24, 48 and 72 hours. Cell viability was examined by MTT assay after 24, 48 and 72 hours. Apoptosis was determined in cells treated with emodin (0, 10, 25 and 50 µM) using flow cytometric assay. Alterations in expression of apoptotic-related genes (Caspase 3, 8, 9, Bcl2 and Bax) were determined by real time PCR. Caspase 3 activity was measured using a colorimetric assay.
Emodin had inhibitory effects on the proliferation of SKBR3 cells with IC50 value of 25 µM. Emodin induced apoptosis and increased the mRNA expression of Caspase 3, 8, 9 and Bax and decreased the mRNA expression of Bcl2 in SKBR3 cells. It also increased the activity of Caspase 3.
Emodin had an inhibitory effect on the growth of SKBR3 cell line in a dose and time dependent manner. This study indicated that emodin induces apoptosis in SKBR3 cells through the alterations of the expression of apoptosis-related genes and increases the activity of Caspase 3.

Fatty acid synthase is a multifunctional protein that catalyzes de novo synthesis of long-chain fatty acids. FASN expression is higher in HER2-positive cells, such as SKBR3 and MCF-7/HER2 cells, than in MCF-7 cells, which express lower HER2 levels. Curcumin, a yellow-colored hydrophobic polyphenol derived from the rhizome turmeric, significantly suppressed growth of human breast cancer cells. In this study, we assessed the effect of curcumin on expression and activity of fatty acid synthase in SK-BR-3 breast cancer cells.
In this study, we decided to determine the effects of Curcumin on Fatty Acid Synthase expression and enzyme activity in breast cancer cell line SKBR3.
We assessed the cytotoxicity effect of curcumin in SK-BR-3 cells by MTT. Apoptosis was performed by flow cytometry. FAS activity was measured by a spectrophotometer at 340 nm of NADPH absorption. Fatty acid synthase gene expression was analyzed by real-time PCR.
Curcumin could decrease cell viability and induce apoptosis in SK-BR-3 cells. Curcumin also reduces the enzyme activity and expression of fatty acid synthase.
It is possible that inhibitory effects of curcumin on FAS may induce apoptosis in SK-BR-3 breast cancer cells.

Iron chelation therapy is used to reduce iron overload development due to its deposition in various organs such as liver and heart after regular transfusion. In this review, different iron chelators implicated in treatment of iron overload in various clinical conditions have been evaluated using more up-to-date studies focusing on these therapeutic agents. Deferoxamine, Deferiprone and Deferasirox are the most important specific US FDA-approved iron chelators. Each of these chelators has their own advantages and disadvantages, various target diseases, levels of deposited iron and clinical symptoms of the afflicted patients which may affect their selection as the best modality. Taken together, in many clinical disorders, choosing a standard chelator does not have an accurate index which requires further clarifications. The aim of this review is to introduce and compare the different iron chelators regarding their advantages and disadvantages, usage dose and specific applications.

The non-enzymatic carbamylation of low density lipoprotein (LDL) is a naturally occurring chemical modification of apolipoprotein B as a result of condensation between lysine residues and cyanate derived from urea. Carbamylated LDL is poorly recognized by LDL receptors and initiates different processes that can be considered proatherogenic. Thus, LDL carbamylation may contribute to the increased risk of atherosclerosis in patients with kidney failure. The objective of this study was to investigate in vitro effects of flavonoids on LDL carbamylation. LDL was isolated from plasma using ultracentrifuge technique with a single step discontinuous gradient. Then, cyanate was added to LDL and LDL carbamylation level was estimated in absence and presence of flavonoids by a colorimetric method at 530 nm. The results of this study showed that a number of flavonoids including rutin, catechin, morin, myricetin, kaempferol, taxifolin, luteolin, naringin and quercetin decreased LDL carbamylation in a dose dependent manner. Also, it was demonstrated that these nutrients decreased electrophoretic mobility of carbamylated LDL. Based on the results obtained in this study, it is suggested that flavonoids are able to inhibit LDL carbamylation (probably by scavenging cyanate ions) and thus, may have a role in ameliorating atherosclerotic risk of patients with kidney failure.