Based on the bending experiment for two-span continuous post-tension beams with unbounded tendons and externally applied CFRP sheets, the analysis of the stress increment of unbonded tendons is monitored in the loading process. Since self-compacting concrete (SCC) is a suitable innovation,, understanding the implementation of this type of concrete on the ultimate unbonded tendon stress is critical. For these aims, results of four continuous un-bonded post-tensioned I-beams in two groups were cast and monitored by electrical strain gauges and are presented here. In the first group, the beams (UPN1-12, SUPN1-12) consisted of high strength normal concrete (HSNC), while in the second group (UPS1-12, SUPS1-12) high strength self-compacting concrete (HSSCC) were tested. The beams are made which are compared with the theory proposed by different codes, and a preliminary modification is given for each code equation. The results of standard error of estimate Sy/x, indicates that for two types of HSCs (strengthened and non-strengthened beams), the ACI 318 2011 provides better estimates than AASHTO-2010 model, whereas this model provides better estimates as compared toBS 8110-97.Comparison of increase in experimental ultimate tendon stress of beams indicates that the increase in tendon stress at ultimate state in strengthened beams is lower than that in nonstrengthened beams cast with HSCs.

Objective: To study the therapeutic effect of mesenchymal stem cells (MSC) on induced liver fibrosis in mice model and to uncover its mechanism.Materials and Methods: we infused GFP+ MSCs of male into the tail vein of female mice that received CCl4 injection biweekly to induce liver fibrosis. MSC which were derived from bone marrow obtained from femoral and tibial bones, isolated and proliferated in culture. They were characterized morphologically and by their potential of differentiation to osteo and adipo lineage. Animals were divided into 6 groups: control, CCl4 4 week, CCL4 8 week, CCl4 4week plus MSC, CCl4 8 week plus MSC, CCL4 plus opportunity to regeneration. Liver tissue was examined histopathologically and by software to quantify collagene deposition as the stage of liver fibrosis. Lipid peroxidation was quantified as a marker of liver injury level. Gene expression ratio of the collagen (type I), TIMP1, MMP-9, MMP-13, alph SMA was detected. Immunostaining were done to show homing and differentiation to hepatocyte of the cells and presentation of Hepatic stellate cells (HSC) liver functions (serum ALT and AST) were estimated for all groups.Results: Quantitative RT-PCR analysis showed administration of MSCs has a significant antifibrotic effect as evidenced by the significant decrease in liver collagen and increase MMP13 gene expression in the CCl4/MSC group compared to the CCl4 group, 4 weeks after transplantation. The expression of αSMA (smooth muscle actin) and TIMP also reduced in CCl4/MSC group. However, this was statistically nonsignificant. Additionally, the expression of MMP9 significant increase in CCl4 treated groups; however, there was no significant change after MSC injection. The reduction in liver collagen confirmed histopathologically by quantitative analysis. Moreover, lipid peroxidation content in transplanted group decreases significantly. Immunostaining of transplanted cells showed GFP-positive cells in the liver and some of them expressed albumin or αSMA.Conclusion: MSCs can enhance recovery of CCl4-injured mouse liver through their influence in reduction collagen deposition by possible effect on matrix metalloptoteases and their capacity to differentiate into hepatocyte-like cells.

Aim: The aim of this study was to determine the effect of inhibition of TGF- b /smad signaling on the expression profiles of miR-335, miR-150, miR-194, miR-27a, miR-199a of hepatic stellate cells (HSCs).Background: Liver fibrosis is excessive deposition of extracellular matrix proteins due to ongoing inflammation and HSC activation that occurs in most types of chronic liver diseases. Recent studies have shown the importance of microRNAs in the pathogenesis of chronic liver diseases.Methods: In this study, for inhibition of TGF- b smad-signaling pathway, expressing Smad4 shRNA plasmids were transfected into HSCs. Subsequently, using Real Time-PCR, we measured the expression levels of miR-335, miR-150, miR-194, miR-27a and miR-199a.Results: Gene expression analysis showed that downregulation of Smad4 by vector Smad4shRNA significantly increased the expression levels of miR-335 (P<0.01) and miR-150 (P<0.001) and decreased the expression level of miR-27a (P<0.05).Conclusion: The results of this study suggest that blocking TGF-b smad-signaling can also differentially modulate microRNA expression in support of activation and fibrogenesis of HSCs.

Background: Efficient induction of fetal hemoglobin (HbF) is considered as an effective therapeutic approach in beta thalassemia. HbF inducer agents can induce the expression of γ-globin gene and produce high levels of HbF via different epigenetic and molecular mechanisms. Thalidomide and sodium butyrate are known as HbF inducer drugs. Material and methods: CD133+ stem cells were isolated from umbilical cord blood of a newborn with minor b-thalassemia in order to evaluate the effects of these two drugs on the in vitro expression of GATA-1 and EKLF genes as erythroid transcription factors. CD133+ stem cells were expanded and differentiated into erythroid lineage and then treated with thalidomide and sodium butyrate and finally analyzed by quantitative real-time PCR. Statistical analysis was performed using student’s t-test by SPSS software. Results: Thalidomide and sodium butyrate increased GATA-1 and EKLF gene expression, compared to the non-treated control (P<0.05). Conclusion: Thalidomide was more efficient than sodium butyrate in augmenting expression of GATA-1 and EKLF genes. It seems that GATA-1 and EKLF have crucial roles in the efficient induction of HbF by thalidomide.

Background: Liver fibrosis is a reversible response to wound-healing that occurs in most forms of chronic liver damage, beginning with the activation of hepatic stellate cells (HSCs). The increased expression of genes, such as beta-converting growth factor (TGF- ) and actin-alpha smooth muscle (-SMA) indicates the activation of HSCs. During liver damage, HSCs are activated and converted to myofibroblasts. As a result, the expression of TGF- and  SMA genes in HSCs increases and leads to liver fibrosis. High fructose intake is known to have harmful effects on human health. Due to the persistent increase in high fructose intake via many beverages and foods in industrialized countries, much concern has been raised about the effect of fructose on liver damage, but its role in activating human HSCs has not been studied. Objectives: We aimed to investigate the effect of high fructose concentration on human HSCs activation by measuring the level of mRNA expression of TGF- and -SMA genes involved in liver fibrosis. Methods: Human HSCs were cultured in Dulbecco’ s Modified Eagle’ s Medium (DMEM) plus 10% Fetal Bovine Serum (FBS) at 37° C in 5% CO2. Cells were incubated in media containing 25 and 30 mM fructose for 48 h. The control group was incubated in DMEM without fructose. The cells were serum-starved for 24 h before treatment. Then, the total RNA was extracted, reversely transcribed into cDNA, and underwent Quantitative Real-time PCR (qRT-PCR). Results: The results indicated that the mRNA expression of TGF- and  SMA genes significantly increased by treating with 25 and 30mMfructose in HSCs when compared to the control group (P < 0. 05). Conclusions: The increase in the mRNA of TGF- and  SMA genes is used as a standard marker for HSC activation, leading to liver fibrosis. The results demonstrated that high fructose concentration could activate HSCs and increase the levels of TGF- and  SMA in these cells. Thus, controlling fructose consumption and identifying the mechanism of fructose action is important to treat and reduce liver injury.