Showing 29 results for Mohammadi
Reza Ebrahimzadeh-Vesal, Roza Azam, Arvin Ghazarian, Mogge Hajesmaeili, Najmeh Ranji, Mohammad Reza Ezzati, Mehrdad Sadri, Mohammad Ali Mohammadi, Siamak Khavandi,
Volume 2, Issue 2 (Vol.2 No.2 Apr 2014)
Abstract
Recurrent pregnancy loss is usually defined as the loss of two or more consecutive pregnancies before 20 weeks of gestation, which occurs in approximately 5% of reproductive-aged women. It has been suggested that women with thrombophilia have an increased risk of pregnancy loss and other adverse pregnancy outcomes. Thrombophilia is an important predisposition to blood clot formation and is considered as a significant risk factor for recurrent pregnancy loss. The inherited predisposition to thrombophilia is most often associated with factor V Leiden mutation, prothrombin G20210A mutation, and methylenetetrahydrofolate reductase C677T and A1298C gene variants. The net effect is an increased cleavage of prothrombin to thrombin and excessive blood coagulation.
Mahdi Zahedpanah, Mojgan Shaiegan, Seyed Hamidollah Ghaffari, Mohsen Nikbakht, Mahin Nikugoftar, Saeed Mohammadi,
Volume 4, Issue 2 (Vol.4 No.2 Apr 2016)
Abstract
Background: Interfering with cell proliferation and survival is a critical role for antineoplastic drugs leading to cell death through induction of apoptosis. Alternative treatments with herbal extracts offer insights into acute myeloid leukemia (AML) therapy. Parthenolide (PTL), an extract from feverfew, induces apoptosis in primary human leukemia stem cells (LSCs) and bulk leukemic cell populations. Osteopontin (OPN) preserves cell viability in response to anticancer agents and its receptors could be utilized for therapeutic targeting of cancer cells.
Methods: U937 cells were cultured in RPMI 1640 with concentrations of 2, 4, 6, 8, and 10 μM PTL for 20-24 hours for MTT assays. Apoptosis assays were performed with Annexin V-Alexa Fluor-488/PI as Annexin V+/PI- and Annexin V+/PI+ to measure early and late apoptosis, respectively. Quantitative real-time PCR was used to measure OPN gene expression using the 2-∆∆Ct method. The PTL–treated cells were stained with FITC-CD38 antibody for flow cytometry analyses. Data were compared using one-way analysis of variance (ANOVA) by SPSS 19.
Results: Parthenolide inhibited growth of U937 cells with IC25 and IC50 values of 4 and 5.8 µM, respectively. Death induction with PTL was apoptotic. Flow cytometry showed a significant decrease in the percentage of CD38+ U937 cells in response to PTL. Osteopontin gene expression decreased in response to PTL.
Conclusions: PTL induced apoptosis and reduced OPN gene expression in U937 cells.
Mojgan Mohammadi, Mohammad Hossein Gozashti, Majid Aghadavood, Mohammad Reza Mehdizadeh, Mohammad Mahdi Hayatbakhsh,
Volume 6, Issue 1 (Vol.6 No.1 Oct 2017)
Abstract
Background: Several components of metabolic syndrome (MetS) facilitate its diagnosis, including abdominal obesity, hyperlipidemia, high blood pressure, and insulin resistance. The production of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6) seem to be associated with MetS components. The aim of this study was to evaluate the correlation between the serum levels of TNFα and IL-6 with metabolic syndrome and its components.
Methods: This case-control study investigated a total of 250 subjects, comprising 125 healthy controls from the Kerman Blood Transfusion Organization and 125 metabolic syndrome patients. Serum IL-6 and TNF-a levels were measured using the ELISA technique.
Results: There was a significant increase in the serum levels of TNF-a and IL-6 in patients with metabolic syndrome compared with the controls. However, a lack of correlation between MetS components and TNF-a and IL-6 serum levels was detected.
Conclusions: Patients with MetS had significantly raised serum IL-6 and TNF-a levels compared with the controls, supporting the evidence that inflammation plays an important role in the immunopathogenesis of the disease. Additionally, serum levels of IL-6 and TNF-a are suggested as valuable predicting factors for MetS. The lack of association between IL-6 and TNF-a serum levels and MetS components remains to be investigated by further research.
Farideh Hosseinzadeh, Saeed Mohammadi, Foroogh Nejatollahi,
Volume 6, Issue 1 (Vol.6 No.1 Oct 2017)
Abstract
Background: Cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) molecules are expressed on T-cells and inhibit their function by inhibiting activation of subsequent T-cell molecular pathways. Blocking of CTLA-4 inhibits the growth of malignant tumor cells. Anti-CTLA-4 monoclonal antibodies activate the immune system against cancer. Due to several advantages of single-chain antibodies (scFvs) compared to monoclonal antibodies in cancer immunotherapy, specific anti-CTLA-4 scFvs (single-chain variable fragment) were selected in this study.
Methods: A phage antibody display library of scFvs was analyzed and a panning process was performed against an immunodominant epitope of CTLA-4. PCR and DNA fingerprinting were used to differentiate the specific clones. The specificity of the selected clones was investigated by phage ELISA (Enzyme-linked immunosorbent assay).
Results: Two specific clones with frequencies of 35 and 20% were identified. The clones reacted with the corresponding epitope on ELISA, while no reactivity was observed with an unrelated peptide, M13KO7 helper phage, unrelated scFvs, or no peptide as negative controls.
Conclusions: Targeted therapy against cancer markers is an ideal treatment strategy. Specific human anti-CTLA-4scFvs were selected in this study. These scFvs bound the related epitope. These antibodies have the potential to be used for targeted therapy, where the blocking of CTLA4 receptor is needed. The study suggests further evaluation of the selected scFvs to reveal the effects of the selected antibodies.
Abbas Yousefinejad, Fereydoon Siassi, Mohammad Hassan Javanbakht, Hamed Mohammadi, Ehsan Ghaedi, Mahnaz Zarei, Ehsan Djalali, Mahmoud Djalali,
Volume 7, Issue 1 (Vol.7 No.1 Oct 2018)
Abstract
Background: Nephrotic syndrome is a disorder caused by kidney damage that results in severe leakage of protein from blood into urine. Hyperlipidemia is one complication of nephrotic syndrome. L-carnitine and genistein can control cardiovascular diseases by causing changes in lipid metabolism and cytokine production. This study was designed to examine the effects of genistein and L-carnitine on serum lipid and cytokine profiles in experimental nephrotic syndrome.
Methods: In this study, 50 male Sprague–Dawley rats were randomly divided into five groups of 10 animals each with similar mean body weights (300±50 g). The five groups were NC (normal-control), PC (patient-control), LC (L-carnitine), G (genistein), and LCG (L-carnitine-genistein). Serum HDL-cholesterol (HDL) LDL-cholesterol (LDL), triglyceride, cholesterol, IL-6, and TNF-α were measured. Statistics were analyzed using SPSS 18.0.
Results: At the end of the study, of the patient groups, HDL was significantly greater in the LC than in the PC or G groups (P<0.001). LDL was significantly less in the G than in the PC, LC, or LCG groups (P<0.001). Interleukin-6 was significantly greater in the PC than in the LC, G, or LCG groups, and significantly greater in the LC than in the G group. (P<0.001), but no significant differences were found for triglyceride, cholesterol, or TNF-α between the patient groups.
Conclusions: Genistein had less effect on HDL and triglyceride levels than LC or LCG. Regarding inflammatory cytokines, genistein and L-carnitine had less effect on TNF-α than on IL-6.
Seyed Amir Jalali, Fatemeh Homaei Shandiz, Jalil Tavakol Afshari, Maryam Davarpanah Tanha Ghochan, Amin Reza Nikpoor, Mojgan Mohammadi,
Volume 7, Issue 1 (Vol.7 No.1 Oct 2018)
Abstract
Background: The First apoptosis signal (FAS) and First apoptosis signal ligand (FASL) genes initiate the apoptosis pathway, playing a central role in the tumor growth and metastasis. Gene polymorphisms including -1377 G/A in the promoter region of FAS and -844 C/T in the promoter region of FASL have shown to change the transcription activities of these genes.
Methods: In this study we evaluated association of these polymorphisms with risk of metastasis of breast cancer, in a population selected from Mashhad, Iran. A total of 115 patients with breast cancer and 115 controls were recruited in this case-control study. Polymerase Chain Reaction-based Restriction Fragment Length Polymorphism (PCR-RFLP) was applied for genotyping on extracted DNA from participant’s blood. Unconditional logistic regression was used to estimate cancer risk by calculating odds ratios (OR) and their 95% confidence intervals (95% CIs).
Results: There was no significant association between these genetic polymorphisms and breast cancer risk. Additionally, our results showed no significant influence from the above mentioned gene polymorphisms on metastasis of breast cancer.
Conclusions: These results suggest that the FAS-1377G/A and FASL-844 C/T gene polymorphism don’t have much influence on the susceptibility to metastasis of breast cancer in northeastern Iranian population. Therefore, we suggest to investigate impact of other candidate gene polymorphisms on metastasis of breast cancer for future research.
Mojgan Mohammadi, Shahriar Dabiri, Hamid Reza Mollaei, Samira Rezaee Jouzdani, Maryam Amizadeh, Jamshid Esmailzadeh, Mohammad Reza Baneshi, Aliasghar Arabi Mianroodi,
Volume 7, Issue 2 (Vol.7 No.2 Jan 2019)
Abstract
Background: Recent studies have shown interleukin 4 (IL-4) and 5 lipoxygenase (5-LO) to play an important role in development of nasal polyposis. Investigation into the genetic factors associated with allergic and non-allergic nasal polyposis has been examined for more than fifteen years. Despite these efforts, the genetic factors underlying the development of nasal polyposis have yet to be clearly understood. The current study examined the relationship between C-590T promoter polymorphisms of the IL-4 gene and the presence of nasal polyps. Additionally, we examined the levels of 5-LO expression in nasal polyp tissue and its association with the IL-4 promoter gene polymorphisms.
Methods: A total of 320 subjects were enrolled in the study, of which 256 were healthy controls and 64 were patients with nasal polyps. The Real-Time PCR HRM-based method was used to determine the genotypes of IL-4 C-590T. The expression of 5-LO within the 64 samples of nasal polyp tissue was determined by immunohistochemical staining to examine the association of 5-LO with the IL-4 C-590T genotype.
Results: Genetic analysis showed a significant difference in the frequencies of the IL-4 polymorphisms at C-590T in patients with nasal polyps as compared with controls (p<0.001). No significant difference was seen in the expression of 5-LO among genotypes in patients with nasal polyps (p=0.139).
Conclusions: The results suggest that the inheritance of TT and CT genotypes at the IL-4 C-590T promoter gene is associated with nasal polyps however, there is no association between the expression of 5-LO in nasal polyp tissues and IL-4 C-590T genotypes in patients with nasal polyps.
Mohammad Mahdi Hayatbakhsh, Arezoo Gowhari Shabgah, Saeed Pishgouyi, Jalil Tavakiol Afshari, Hadi Zeidabadi, Mojgan Mohammadi,
Volume 8, Issue 1 (Vol.8 No.1 Apr 2019)
Abstract
Background: Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by altered bowel habits and abdominal pain in the absence of a recognizable structural anomaly. The pathogenesis of IBS has been associated with inflammation and the expression of pro-inflammatory chemokines, such as CCL2 and CCL16. Our study aimed to investigate the relationship between the serum levels of CCL2 and CCL16 and IBS. Additionally, we examined how serum levels of these chemokines relate to IBS subtypes.
Methods: Patients with IBS diagnosed according to the Rome III criteria participated in this study (n= 96). Healthy individuals with no history of allergic, autoimmune, chronic or active gastrointestinal infectious diseases were used as controls (n= 44). The serum levels of CCL2 and CCL16 was measured via enzyme-linked immunosorbent assay (ELISA).
Results: A significant decrease in the serum levels of CCL16 and CCL2 was observed in the patients with IBS. Additionally, the serum levels of CCL16 in IBS patients with diarrhea (D-IBS) was significantly higher than those with the mixed IBS (M-IBS) subtype.
Conclusions: The significant increase in the serum levels of CCL-16 in patients with D-IBS compared to patients with M-IBS suggests that CCL-16 may be used as an immunological biomarker to differentiate between these two subtypes.
Abbas Shapouri-Moghaddam, Mojgan Mohammadi, Hamid Reza Rahimi, Habibolah Esmaeili, Mahmoud Mahmoudi, Mohammad-Hadi Saeed Modaghegh, Jalil Tavakol Afshari,
Volume 8, Issue 2 (Vol.8 No.2 July 2019)
Abstract
Background: Thromboangiitis obliterans (TAO), also known as Burger’s disease, is a devastating disease affecting the arteries and veins of the upper and lower distal limbs most commonly afflicting young male smokers of low socioeconomic status. The expression of human leukocyte antigen (HLA)-A, B and –DRB1 genes have been implicated in the pathogenesis of TAO. Our study aimed to examine the association of different HLA-A, B and –DRB1 genes in TAO patients in the Iranian population.
Methods: A case-control study examining 55 Iranian patients with TAO and 500 healthy subjects was performed in Imam Reza hospital, Mashhad, Iran. The prevalence of major histocompatibility complex (MHC) class I (-A, -B) and class II (-DRB) alleles were determined for each participant.
Results: Our results revealed the HLA-A*03 (odds ratio [OR]=5.394), HLA-A*24 (OR=5.143), HLA-A*31 (OR=4.251), HLA-A*11 (OR=3.034), HLA-B*27 (OR=6.680), HLA-B*15 (OR=3.959), HLA-B*07 (OR=3.698), HLA-B*51 (OR=3.370), HLA-B*44 (OR=3.326), HLA-DRB1*16 (OR=20.583), HLA-DRB1*04 (OR=8.960), HLA-DRB1*14 (OR=3.746), HLA-DRB1*03 (OR=2.303), and HLA-DRB1*15 (OR=2.111) alleles to occur at a significantly higher frequency in TAO patients compared to controls (p<0.05). The HLA-A*25, HLA-A*66, HLA-DRB1*08, HLA-DRB1*10, and HLA-DRB1*12 alleles resulted in infinite OR, and was associated with an increased risk of TAO. However, the alleles HLA-A*30, HLA-B*08, HLA-B*45, HLA-B*46, and HLA-B*53 were associated with a protective role against TAO with an OR = 0.
Conclusions: This is the first study examining the HLA pattern in patients with Burger’s disease in the Iranian population. Our findings have revealed an association between HLA class I and II alleles with TAO.
Hoda Nadimi, Abolghassem Djazayery, Mohammad Hassan Javanbakht, Ahmadreza Dehpour, Ehsan Ghaedi, Hoda Derakhshanian, Hamed Mohammadi, Mahnaz Zarei, Mahmoud Djalali,
Volume 8, Issue 3 (Vol.8 No.3 Oct 2019)
Abstract
Background: Diabetes mellitus and metabolic disorders are a major burden on the healthcare system. Irisin is a novel myokine reported to have beneficial effects on glucose and lipid metabolism. Vitamin D deficiency has been implicated in the development of diabetes and hold a critical role in diabetes-related complications. In the present study, we examined the efficacy of vitamin D supplementation on serum irisin levels, skeletal muscle irisin levels, and the expression of the irisin precursor, FNDC5 (fibronectin-type III domain-containing 5) in type I diabetes mellitus rats.
Methods: Thirty-six adult male Sprague-Dawley rats (150 – 250 g) were randomly divided into four groups: group I: healthy control rats with no treatment (n=8), group II: healthy control rats receiving sesame oil as a placebo (n=8), group III: diabetic rats receiving sesame oil as placebo (n=10), group IV: diabetic rats treated with 4300 IU/kg/week vitamin D (n=10). Diabetes was induced by intraperitoneal (IP) injection of streptozotocin. At the end of the vitamin D intervention blood and triceps muscle samples were collected. RNA was extracted from muscle and real-time PCR was performed to examine FNDC5 gene expression.
Results: Our study showed that the administration of vitamin D (4300 IU/kg/week) in a streptozotocin-diabetic rat model resulted in increased serum vitamin D levels, FNDC5 gene expression and muscle irisin levels. However, the levels of serum irisin were not significantly changed by the administration of vitamin D.
Conclusions: In conclusion, we show that vitamin D supplementation enhances serum vitamin D levels, FDNC5 gene expression and muscle irisin levels in the streptozotocin-diabetic rat model. Our study highlights the potential therapeutic effect of vitamin D supplementation for diabetes mellitus.
Zahra Taheri, Hamid Asadzadeh Aghdaei, Shiva Irani, Mohammad Hossein Modarressi, Zahra Noormohammadi,
Volume 8, Issue 3 (Vol.8 No.3 Oct 2019)
Abstract
Background: Abnormal DNA methylation leading to altered transcription of certain genes occurs frequently in colorectal cancer (CRC). As with protein-coding genes, microRNAs (miRNAs) may be targeted for methylation in CRC; however, the methylation state of miRNA genes in CRC, especially in primary lesions, has not yet been completely elucidated. To understand the impact of DNA methylation on the miR-200c/141 cluster promoter, we investigated the methylation and expression of miR-141 in precancerous lesions and colorectal cancer.
Methods: In this cross-sectional study, 208 colorectal tissue samples, including 34 tumor tissue samples, 60 precancerous lesions with matched normal adjacent tissues, and 20 normal tissue samples, were collected. Promoter methylation of the miR-200c/141 cluster was studied using methylation-specific PCR. MiR-141 expression was examined using quantitative real-time PCR.
Results: Our findings showed that the miR-200c/141 cluster promoter region was most frequently hypermethylated in colorectal tumors and adenomatous polyps, but unmethylated in hyperplastic polyp tissues (P < 0.001). DNA methylation of the miR-200c/141 cluster and the tumor stage were significantly correlated (P = 0.002); however, miR-141 expression difference between the tumor and polyp samples was not significant (p = 0.6).
Conclusions: The DNA methylation status of the miR-200c/141 cluster could serve as a progression marker from benign polyps to colorectal cancer.
Mahdis Ghavidel, Keyvan Tadayon, Nader Mosavari, Kimiya Nourian, Hamid Reza Bahramitaghanaki, Gholam Reza Mohammadi, Mohammad Rashtibaf, Kiarash Ghazvini,
Volume 8, Issue 3 (Vol.8 No.3 Oct 2019)
Abstract
Background: Tuberculosis (TB) still remains endemic worldwide making epidemiological studies essential to mitigating efforts implicated in identifying its source,controlling, and preventing the spread of dangerous strains amongst humans such as Mycobacterium tuberculosis (Mtb).
Methods: In this study, we sought to determine the 6 Mycobacterial Interspersed Repetitive Unit-Variable-Number Tandem Repeat (MIRU-VNTR) loci with high discriminatory powers for Mtb genotypingas well as the loci with the highest and the lowest discriminatory powers for MIRU-VNTR.To conduct our search, we used several databases such as science direct, Embase (Elsevier), Web of Science, Scopus and Medline via PubMed. Searches were performed using key words including: Mycobacterium tuberculosis, MIRU–VNTR, Allele diversity, Genetic diversity and human patient. Finally, 56 articles were selected after filtering out titles, abstracts and full texts.
Results: Loci with high discriminatory powers included MIRU10 and MIRU26, while MIRU2, MIRU20, MIRU24 and ETRD had poor discriminatory powers. According to previous data in the literature, the loci MIRU10, MIRU26, MIRU40, QUB 26, QUB 11b and Mtub21 have high discriminatory powers.
Conclusions:Therefore, these loci recommended for genotyping Mtb to save time and cost and to ensure the production of reliable results.
Sanaz Zebardast, Mehdi Sahmani, Saeed Mohammadi, Farshad Foroughi, Ali Dehghani Fard, Zahra Mohammadi, Sahar Khojastepour, Mehdi Azad,
Volume 8, Issue 4 (Vol.8 No.4 Jan 2020)
Abstract
Background: DNA methylation is an epigenetic modification that has the ability to alter gene expression and function. These epigenetic changes have been associated with the development of cancer. Previous research has found that DNA methylation patterns can predict disease prognosis for patients with Acute Promyelocytic Leukemia (APL). The role of DNMT1 and CDH1 in regulating the extension of cells are studied in this study.
Methods: DNA was extracted from peripheral blood samples of APL patients and treated with bisulfite. DNMT1 and CDH1 gene promoter methylation was subsequently analyzed using methylation-specific PCR (MSP). Real-time PCR was used to measure the expression level of DNMT1 and CDH1 genes.
Results: Partial methylation of the CDH1 gene promoter was detected in 20% of APL patients and an unmethylated status was detected in 80% of patient samples. Additionally, an unmethylated status in the DNMT1 gene promoter was detected in 100% of APL patient samples.
Conclusions: Our study found the CDH1 gene promoter to be unmethylated in almost all APL patients, while the DNMT1 promoter was unmethylated in all APL patients. Furthermore, we observed an increase in both CDH1 and DNMT1 gene expression in APL patients compared to healthy controls. These findings suggest that DNMT1 may not have a specific role in inhibiting CDH1 gene expression in APL. Applying higher resolution techniques would help to better uncover the DNA methylation patterns in patients with APL. Further research is required to determine the role of DNA methylation and CDH1 and DNMT1 gene expression in APL.
Omid Salemi, Zahra Noormohammadi, Fariborz Bahrami, Seyed Davar Siadat, Soheila Ajdary,
Volume 8, Issue 4 (Vol.8 No.4 Jan 2020)
Abstract
Background: It is estimated that one third of the world's population is infected with Mycobacterium tuberculosis (Mtb), the causative agent of Tuberculosis (TB). The BCG vaccine is widely used to fight against TB; however, many question its ability to provide complete protection from Mtb. Recently, the "Region of Difference 1" (RD1) set of genes were shown to be involved in the pathogenesis of Mtb. Downstream of RD1 transcription region, two proteins are encoded, known as EspB and EspC, which were found to contribute to Mtb virulence. In this study these two proteins are targeted as potential vaccine candidates against TB.
Methods: The EspB and EspC Mtb genes were codon-optimized for expression and synthesis in Escherichia coli (E. coli). The amplicons were cloned into a pET21a expression vector and transformed into E. coli BL21(DE3). The expression and purity of the expressed proteins (i.e. rEspC, rEspB and rEspC/EspB) were confirmed by SDS-PAGE and Western blotting. Moreover, BALB/c mice were immunized against Mtb using the recombinant proteins. Finally, the mice sera were analyzed via Western blotting.
Results: EspC, EspB, and EspC/EspB fusion genes were cloned and expressed in E. coli. Both SDS-PAGE and Western blots confirmed the presence and successful purification of the desired proteins. Moreover, antisera produced against the purified recombinant proteins reacted with Mtb proteins.
Conclusions: rEspC, rEspB, and rEspC/EspB could be expressed and purified using an E. coli expression system. The recombinant proteins induced the production of antibodies in BALB/c mice that reacted with Mtb proteins.
Mona Djalali, Mahmoud Djalali, Mina Abdolahi, Hamed Mohammadi, Hajar Heidari, Shayesteh Hosseini, Majid Sadeghizadeh,
Volume 9, Issue 1 (Vol.9 No.1 Apr 2020)
Abstract
Background: This study was designed to investigate the effect of nano-curcumin supplementation on pentraxin 3 (PTX3) gene expression and serum level in migraine patients.
Methods: The present study, performed as a clinical trial, included 38 episodic migraine patients in two groups that received either nano-curcumin or placebo over a two-month period. At the start and the end of the study, PTX3 gene expression and serum levels were measured.
Results: After two months of treatment, PTX3 gene expression and serum levels were both significantly less in the nano-curcumin than in the placebo group (P= 0.01 and P< 0.001, respectively). No significant gene expression differences were found between the two groups.
Conclusions: Curcumin may have a potential inhibitory effect on PTX3 gene expression and serum levels in migraine disease and can be considered as an efficient therapy in migraine management.
Zahra Taheri, Hamid Asadzadeh Aghdaei, Shiva Irani, Mohammad Hossein Modarressi, Zahra Noormohammadi,
Volume 9, Issue 1 (Vol.9 No.1 Apr 2020)
Abstract
Background: Epigenetic changes in CpG islands of the promoter regions of homeostasis-related genes, including nuclear factor erythroid 2-related factor 2 (NRF2), have been shown to hold a significant role in the development of colorectal cancer. Therefore, we aimed to examine the DNA demethylation pattern of the NRF2 promoter region in cancerous lesions from patients with colorectal cancer and the association of methylation status with clinicopathological features in the Iranian population.
Methods: In this cross-sectional study, 114 colorectal tissue samples were collected. These samples included: 34 tumour tissue samples, 60 precancerous polyps, and 20 normal tissue samples. The promoter methylation status of the NRF2 gene was examined using methylation-specific PCR. Additionally, the relationship between the methylation status and the clinicopathological features was investigated.
Results: The frequency of NRF2 demethylation in the tumour samples was significantly higher compared to the polyp tissues (p= 0.003) and normal tissue (p= 0.009), indicating that cancerous colorectal tissues exhibit increased demethylation of the NRF2 promoter. After examining the demethylation status of tissue samples, the clinicopathological features were compared to the demethylation results. No significant association was found between NRF2 promoter demethylation and the clinicopathological features of patient samples.
Conclusions: Our findings suggest that the epigenetic modifications leading to NRF2 demethylation found in colorectal tumour samples may contribute to cancer progression from precancerous polyps to cancerous lesions.
Ahmad Lotfi Garavand, Mohammad Mohammadi, Sara Mohammadzadeh,
Volume 9, Issue 1 (Vol.9 No.1 Apr 2020)
Abstract
Background: The tumor suppressing protein p53 and its downstream effector p21 play important roles in cell cycle regulation. Deficiency or deactivation of these proteins as a result of gene alterations has been indicated in several cancers. Such genetic variations could be considered as susceptibility indicators in acute lymphocytic leukemia (ALL). Therefore, we investigated the associations between ALL risk and TP53 codon 72, p21 codon 31, and MDM2 SNP309 polymorphisms in an Iranian population.
Methods: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine the MDM2 T309G (rs2279744), TP53 codon Arg72Pro (rs1042522), and p21 Ser31Arg (rs1801270) single nucleotide polymorphisms (SNPs). This study was performed in 115 ALL patients and 115 healthy controls in Khuzestan province in southwest Iran.
Results: In the control group and ALL patients, p21 Ser/Arg, and MDM2 TG and GG genotypes were associated with significant 1.81-fold (95% confidence interval CI= 1.008-3.267; P ˂ 0.05), 11.07-fold (95% CI= 5.10-24.05; P < 0.0001), and 19.41-fold (95% CI= 8.56-43.99; P < 0.0001) increased risks for ALL, respectively. The TP53 72 Arg allele was significantly more prevalent in ALL patients (56.96%) than in control subjects (47.39%), and was significantly associated with ALL (OR= 1.47; 95% CI = 1.017-2.121, P < 0.05).
Conclusions: The MDM2 T309G and the p21 Ser31Arg SNPs indicate a significantly increased risk for developing ALL in Khuzestan province.
Hanieh Beikmohammadi, Iman Pouladi, Mohammad Reza Zolfaghari, Mohammad Niakan,
Volume 9, Issue 2 (Vol.9 No.2 Jul 2020)
Abstract
Background: Mycoplasma pneumoniae is one of the widespread causes of community-acquired pneumonia (CAP). Over recent years, the widespread use of macrolides has led to the emergence of macrolide-resistant M. pneumoniae (MRMP) resulted from mutations at specific positions of domain V of the 23S rRNA gene.
Methods: We collected 100 samples of throat swabs from patients with respiratory infections. After extraction of DNA from bacterial cell cultured in PPLO broth media using Roche kit (Germany), the PCR was performed on specific samples of M. pneumoniae using specific primers for 23S rRNA gene. Afterwards, for positive samples, minimum inhibitory concentration (MIC) was determined using the broth microdilution with Clarithromycin. Finally, the PCR product was sequenced to detect mutations related to macrolide resistance in domain V of 23S rRNA.
Results: According to the analysis of the sequenced PCR product of M. pneumoniae 23S rRNA gene using Clustalw2 online software, one of the samples were shown to have a mutation at A2431G and G2491A positions. The MIC measurement also revealed that all isolates were sensitive to Clarithromycin, and there was no macrolide resistance to Clarithromycin in all isolates.
Conclusion: Sequence analysis of the 23S rRNA gene in M. pneumoniae, revealed no macrolide resistance of M. pneumoniae to Clarithromycin. Thus, the use of these antibiotics should be restricted to prevent the development of macrolide-resistant M. pneumoniae in Iran.
Pantea Mohammadi, Mina Zangeneh, Hamid-Reza Mohammadi-Motlagh, Fatemeh Khademi,
Volume 9, Issue 3 (Vol.9 No.3 Oct 2020)
Abstract
Background: Non-Hodgkin’s lymphomas comprise the most common hematological cancers worldwide and consist of a heterogenous group of malignancies affecting the lymphoid system. Treatment of non-Hodgkin’s lymphoma has been significantly enhanced with the addition of Rituximab to the standard chemotherapy regimen. However, even with the advancement of treatment patients continue to relapse and develop resistance to Rituximab, rendering subsequent treatments unsuccessful. The use of novel drugs with unique antitumor mechanisms has gained considerable attention. In this study, we explored the in vitro anti-cancer effects of the combined therapy of Rituximab and Nisin on human Burkitt’s lymphoma cells.
Methods: The human Burkitt’s lymphoma cells lines, Raji and Daudi, were treated with Nisin, Rituximab, or a combination of the two agents at various concentrations. Cytotoxicity following treatment was determined using cell viability assay. The degree of apoptosis was verified via flow cytometric analysis using FITC annexin V/PI staining.
Results: Our findings show that the combined treatment of Rituximab and Nisin results in a more significant reduction in the survival of Raji and Daudi Burkitt’s lymphoma cells, compared to Nisin or Rituximab treatment alone. Additionally, our results indicate that Nisin can induce a significant degree of apoptosis in the Burkitt’s lymphoma cells compared to the negative controls. However, the addition of Nisin to the Rituximab treatment synergistically enhances the apoptotic antitumor effect.
Conclusions: This study demonstrates the synergistic antitumor effect of Nisin treatment in vitro to enhance tumor cell apoptosis and the potential value of Nisin as an adjunct therapy in the treatment of lymphoma.
Bahman Mirzaei, Ryhaneh Babaei, Mohammad Reza Haghshenas, Mohammad Reza Hagshenas, Fatemeh Mohammadi, Pegah Homayoni, Ebrahim Shafaei,
Volume 10, Issue 1 (Vol.10 No.1 Apr 2021)
Abstract
Background: Staphylococcus aureus as a causative agent of hospital-acquired infections has been considered as the primary concern in biomaterial-related infections (BAIs).
Methods: Following the purification of polysaccharide intercellular adhesion (PIA) as an efficient macromolecule in biofilm formation in the native condition, recombinant S. epidermidis surface-exposed rSesC protein, with the most homology to clumping factor A (ClfA) in S. aureus was cloned and expressed in a prokaryotic host as well. Fourier transform infrared spectrometry (FTIR) and Western blotting procedure analyzed purified PIA and protein, respectively. Then, the immune response was evaluated by measuring total IgG titers. Moreover, the capacity of Anti-biofilm forming activity of arisen antibodies to a biofilm-forming S. aureus strains was assessed by the semi-quantitative micro-plate procedure.
Results: Data showed that the total IgGs were boosted in mice immunized sera. By performing an inhibition assay, the biofilm inhibitory effect of secreted antibodies to test strain was observed. Arisen antibodies against the mixture significantly were more potent than PIA and rSesC, when comparing individual antigens in a biofilm inhibition assay.
Conclusions: immunization of mice with mentioned antigens especially a mixture of them, could eliminate the biofilm formation process in S. aureus. Hopefully, this study corresponds to the suggestion that the immunization of mice with PIA and rSesC candidate vaccines could protect against S. aureus infection.
