Tehrān, Iran
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PubMed | Sarem Womens Hospital, Ahvaz Jundishapur University of Medical Sciences, Tarbiat Modares University and Shahid Beheshti University of Medical Sciences
Type: Journal Article | Journal: International journal of hematology-oncology and stem cell research | Year: 2014

Potent induction of fetal hemoglobin (HbF) production results in alleviating the complications of -thalassemia and sickle cell disease (SCD). HbF inducer agents can trigger several molecular signaling pathways critical for erythropoiesis. Janus kinase/Signal transducer and activator of transcription (JAK/STAT), mitogen activated protein kinas (MAPK) and Phosphoinositide 3-kinase (PI3K) are considered as main signaling pathways, which may play a significant role in HbF induction. All these signaling pathways are triggered by erythropoietin (EPO) as the main growth factor inducing erythroid differentiation, when it binds to its cell surface receptor, erythropoietin receptor (EPO-R) HbF inducer agents have been shown to upregulate HbF production level by triggering certain signaling pathways. As a result, understanding the pivotal signaling pathways influencing HbF induction leads to effective upregulation of HbF. In this mini review article, we try to consider the correlation between HbF inducer agents and their molecular mechanisms of -globin upregulation. Several studies suggest that activating P38 MAPK, RAS and STAT5 signaling pathways result in efficient HbF induction. Nevertheless, the role of other erythroid signaling pathways in HbF induction seems to be indispensible and should be emphasized.


PubMed | Sarem Womens Hospital, Tabriz University of Medical Sciences, Zanjan University of Medical Sciences and Tarbiat Modares University
Type: Journal Article | Journal: Cell journal | Year: 2015

Runt-related transcription factor 2 (RUNX2) and osterix (OSX) as two specific osteoblast transcription factors and distal-less homeobox 5 (DLX5) as a non-specific one are of paramount importance in regulating osteoblast related genes including osteocalcin, bone sialoprotein (BSP), osteopontin and collagen type I1. The present study sets out to investigate whether epigenetic regulation of these genes is important in osteoblastic differentiation of mesenchymal stem cells (MSCs).In this experimental study, MSCs were differentiated to osteoblasts under the influence of the osteogenic differentiation medium. DNA and RNA were extracted at days 0, 7, 14 and 21 from MSCs differentiating to osteoblasts. Promoter regions of RUNX2, OSX, DLX5 and BSP were analyzed by methylation-specific PCR (MSP). Gene expression was analyzed during osteoblastic differentiation by quantitative real-time polymerase chain reaction (PCR).MSP analysis revealed that promoter methylation status did not change in RUNX2, DLX5 and BSP during MSC osteoblastic differentiation. In contrast, OSX promoter showed a dynamic change in methylation pattern. Moreover, RUNX2, OSX, DLX5 and BSP promoter regions showed three different methylation patterns during MSC differentiation. Gene expression analyses confirmed these results.The results show that in differentiation of MSCs to osteoblasts, epigenetic regulation of OSX may play a leading role.


PubMed | Golestan University of Medical Sciences, Tarbiat Modares University, Tehran University of Medical Sciences, Shahid Beheshti University of Medical Sciences and 2 more.
Type: Journal Article | Journal: International journal of hematology-oncology and stem cell research | Year: 2015

Early diagnosis and treatment of leukemia patients remains a fundamental aim in clinical oncology, especially in developing country. Present study highlights the basic requirements of these patients in Iran. Better understanding of these issues may lead to improve the healthcare standards toward leukemia diagnosis and treatment.This descriptive study included 101 specialists in hematology-oncology and pathology serving in oncology centers. The participants were then asked to fill out a standard questionnaire on the issues around diagnosis and treatment of blood malignancies.According to specialists, unfair distribution of facilities across the country, delayed diagnosis of disease, absence of psychological support for patients, and insufficient financial support were the main reasons of inappropriate diagnosis and treatment in leukemia patients.Our results show that making an amendment to health policies by preparing well-equipped medical centers in all provinces, improving the morale of patients through consultation during the process of treatment, and above all, subsiding leukemia patients financial problems will promote the health standard regarding the leukemia diagnosis and treatment in Iran.


Saremi A.,Sarem Womens Hospital | Saremi A.,Sarem Cell Research Center | Bahrami H.,Sarem Womens Hospital | Bahrami H.,Sarem Cell Research Center | And 5 more authors.
Reproductive BioMedicine Online | Year: 2014

The advised treatment for severe adenomyosis is hysterectomy, but for patients wishing to preserve their uterus, novel conservative surgery, adenomyomectomy, can be performed. The technique needs to be developed to reduce spontaneous uterine rupture, adhesion and recurrence rates. This study aimed to investigate the safety and therapeutic outcomes of adenomyomectomy. Prospectively, 103 Iranian patients with documented severe adenomyosis were candidates for adenomyomectomy over a period of 7 years (from April 2004 to March 2011). The surgical procedure involved resection of adenomatosis lesions with a thin (≤0.5 cm) margin (wedge-shaped removal) after sagittal incision in the uterine body. Reconstruction of the layers was performed and inverted sutures were used for the serosal layer ends. Of 103 patients, 55.34% presented with infertility, 16.50% with IVF failure, 8.74% with recurrent abortion and 19.42% with abnormal uterine bleeding. Of 70 patients who attempted pregnancy, naturally (n = 21) or by assisted reproduction treatment (n = 49), 30% achieved a clinical pregnancy, and 16 resulted in a full-term live birth. Dysmenorrhoea and hypermenorrhoea were reduced post surgery. Only one patient had relapsed adenomyosis. Adenomyomectomy is a conservative and effective treatment for adenomyosis. This study describes an efficient procedure to treat severe adenomyosis. Adenomyosis is uterine thickening that occurs when endometrial tissue, which normally lines the uterus, moves into the outer muscular walls of the uterus. The advised treatment for the severe forms of adenomyosis is hysterectomy (removal of the patient's uterus), but for the patient who wishes to preserve her uterus, a novel conservative surgery referred to as 'adenomyomectomy' (removal of the abnormal tissues) can be performed. This technique must be developed for reduction of spontaneous uterine rupture, adhesions and recurrence rate. This study aims to investigate the safety and therapeutic outcomes of adenomyomectomy. Prospectively, 103 Iranian patients with documented severe adenomyosis were candidates for adenomyomectomy over a period of 7 years (from April 2004 to March 2011). The surgical procedure was resection of adenomatosis lesions with a thin margin. Of 103 patients, 55.34% presented with infertility, 16.50% with IVF failure, 8.74% with recurrent abortion and 19.42% with abnormal uterus bleeding. Of 70 patients who attempted pregnancy either naturally (n = 21) or using assisted reproduction technology (n = 49), 30% became pregnant, and 16 pregnancies reached full term. There was a significant reduction in dysmenorrhoea and hypermenorrhoea. Only one patient had relapsed adenomyosis. Based on these results, we conclude that adenomyomectomy is the conservative and effective option to treat adenomyosis with preservation of the uterus. The procedure described in this study can be an efficient procedure to treat severe adenomyosis. © 2014, Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.


Ahmadbeigi N.,Stem Cell Technology Research Center | Ahmadbeigi N.,Tarbiat Modares University | Shafiee A.,Stem Cell Technology Research Center | Seyedjafari E.,Stem Cell Technology Research Center | And 7 more authors.
Cell Proliferation | Year: 2011

Objectives: Bone marrow-derived mesenchymal stem cells (BM-MSC) have been widely used for cell therapy and tissue engineering purposes. However, there are still controversies concerning safety of application of these cells after in vitro expansion. Therefore, we aimed to investigate the characteristics of rabbit BM-MSC during long-term culture.Materials and methods: In this study, we have examined growth kinetics, morphological changes, differentiation potential and chromosomal abnormalities, as well as tumour formation potential of rabbit BM-MSC in long-term culture.Results and conclusion: We found that shortly after isolation, proliferation rate of rabbit BM-MSC decreases until they enter a dormant phase. During this period of quiescence, the cells are large and multinucleate. After some weeks of dormancy we found that several small mononuclear cells originated from each large multinucleate cell. These newly formed cells proliferated rapidly but had inferior differentiation potential. Although they were immortal, they did not have the capability for tumour formation in soft agar assay or in nude mice. This is the first report of spontaneous, non-tumorigenic immortalization of BM-MSC in rabbits. The phenomenon raises more concern for meticulous monitoring and quality control for using rabbit BM-MSC in cell-based therapies and tissue engineering experiments. © 2010 Blackwell Publishing Ltd.


Fallahpour M.,Sarem Womens Hospital | Hafizi A.,Shahid Beheshti University | Fouladgar A.,Sarem Womens Hospital | Rajabian B.,Tehran University of Medical Sciences
Archives of Iranian Medicine | Year: 2012

Microthrombi formation and hemolytic anemia are signs of hemolytic-uremic syndrome (HUS) that result from platelet consumption and red blood cell (RBC) destruction due to vascular damage. HUS manifests as a triad of signs: micro-angiopathic hemolytic anemia, thrombocytopenia, and uremia. Prenatal asphyxia (PA) also leads to renal insufficiency and vascular damage. There is an overlap between the clinical presentation of PA and neonatal atypical HUS. We have reported the case of a neonate with a primary diagnosis of PA and clinical presentation of acute renal failure (ARF), anemia (Hb = 10 g/dl) and thrombocytopenia (Plt = 80000). His APGAR scores were 1 (1 minute), 3 (5 minutes), and 7 (10 minutes). A peripheral blood smear (PBS) was performed, which contained schistocytes (32%) with helmet and burr cells. The neonate's cord blood gas values were: pH of 7.07, HCO3 = 11mmol/L, and CO2 = 57mmHg. The first two days of life, he was anuric with elevated BUN and Cr (2.1mg/dL) levels. Complement (C3) was within normal limits at 0.65 g/L (0.89 - 1.87 g/L), however C4 was below the lower limit of normal at 0.14 g/L (0.16 - 0.38 g/L). We ruled out other causes of PA such as maternal illness, placenta abnormalities and infections (TORCH). We hypothesized that atypical neonatal HUS can progress to PA because of the presence of severe anemia and microthrombi formation.


Fard A.D.,Sarem Womens Hospital | Hosseini S.A.,Ahvaz Jundishapur University of Medical Sciences | Shahjahani M.,Tarbiat Modares University | Salari F.,Ahvaz Jundishapur University of Medical Sciences | Jaseb K.,Ahvaz Jundishapur University of Medical Sciences
International Journal of Hematology-Oncology and Stem Cell Research | Year: 2013

Objective: The use of fetal hemoglobin (HbF) inducer drugs is considered as a novel approach in treatment of β-hemoglobinopathies, especially β- thalassemia and sickle cell disease. HbF inducers including hydroxyurea, histone deacetylase (HDAC) inhibitor agents such as sodium butyrate, azacitidine, decitabine and new immunomodulator drugs like pomalidomide, lenalidomide and thalidomide can reduce α-globin chain production in erythroid progenitors and improve α: β chain imbalance, the most crucial complication of β-thalassemia. Materials and Methods: In this article, we reviewed more than 40 articles published from 1979 to 2012 in the field of fetal hemoglobin augmentation. Results: Recent studies suggest the synergistic effect of drug combinations in efficient induction of fetal hemoglobin and gene over-expression. Conclusion: It seems that drugs which act with different molecular and epigenetic mechanisms have proper synergistic effects in fetal hemoglobin induction and gene over-expression.


PubMed | Sarem Womens Hospital, Tarbiat Modares University, Shahid Chamran University and Ahvaz Jundishapur University of Medical Sciences
Type: Journal Article | Journal: International journal of hematology-oncology and stem cell research | Year: 2014

Hemoglobinopathy and thalassemia are prevalent genetic disorders throughout the world. Beta thalassemia is one of these disorders with high prevalence in Iran, especially in Khuzestan province. In this study, the rate of different mutations in -globin gene for prenatal diagnosis in fetal samples was evaluated.In this experimental pilot study, 316 fetal samples (chorionic villus or amniotic fluid) suspicious to hemoglobin disorders were enrolled. Afterwards, DNA was extracted and PCR and DNA sequencing were used for evaluation of different mutations in -globin gene.Amongst 316 samples evaluated for prenatal diagnosis, 180 cases (56.8%) were carrying at least one mutated gene of -thalassemia. In addition, results showed that CD 36-37 (- T) and IVS II-1 (G > A) polymorphisms are the most prevalent polymorphisms of -thalassemia in Ahvaz city with 13.9% and 10.1% rates, respectively.Using molecular tests for prenatal diagnosis is considered an efficient approach for reducing the birth of children with hemoglobinopathy and identification of prevalent mutations in each region.


PubMed | Sarem Womens Hospital, Ahvaz Jundishapur University of Medical Sciences and Tarbiat Modares University
Type: Journal Article | Journal: International journal of hematology-oncology and stem cell research | Year: 2014

The use of fetal hemoglobin (HbF) inducer drugs is considered as a novel approach in treatment of -hemoglobinopathies, especially - thalassemia and sickle cell disease. HbF inducers including hydroxyurea, histone deacetylase (HDAC) inhibitor agents such as sodium butyrate, azacitidine, decitabine and new immunomodulator drugs like pomalidomide, lenalidomide and thalidomide can reduce -globin chain production in erythroid progenitors and improve : chain imbalance, the most crucial complication of -thalassemia.In this article, we reviewed more than 40 articles published from 1979 to 2012 in the field of fetal hemoglobin augmentation.Recent studies suggest the synergistic effect of drug combinations in efficient induction of fetal hemoglobin and gene over-expression.It seems that drugs which act with different molecular and epigenetic mechanisms have proper synergistic effects in fetal hemoglobin induction and gene over-expression.


PubMed | Sarem Womens Hospital, Zahedan University of Medical Sciences, Tarbiat Modares University and Ahvaz Jundishapur University of Medical Sciences
Type: Journal Article | Journal: International journal of hematology-oncology and stem cell research | Year: 2014

-thalassemia considers worldwide public health disorders. Novel fetal hemoglobin inducer agents such as thalidomide and sodium butyrate have been attended for ameliorating clinical complications of such disorders.We used thalidomide and sodium butyrate for increasing the level of fetal hemoglobin in erythroid progenitors. Briefly, after isolation of CD133+ stem cells from umbilical cord blood and differentiation into erythroid lineage, erythroid progenitors were treated with thalidomide and sodium butyraye as single and combination. H3K4 histone methylation was evaluated following fetal hemoglobin induction using chromatin immuno percipitation (ChIP) technique.The results of this study showed that the effect of thalidomide on increasing of H3K4 methylation was highest compared to sodium butyrate and combination of both agents (p < 0.05).Consequently, our study of the epigenetic modification of the -globin suggests that histone H3K4 dimethylation are significant for the regulation of developmental stage-specific expression of the -globin genes.

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