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مقالات رزومه همایون دولتخواه

  • MohammadHossein Somi*, Homayun Dolatkhah, Ahmad Movahedian, Ahmad Mirza Aghazade, Ali Esfahani, Neda Dolatkhah, Arash Khaki
    Background & Aims

     The use of some active factors in diet is regarded as an attractive approach to prevent and to treat certain types of cancers. Accordingly, the main objective of this study was to evaluate the effect of PUFAs oral administration along with chemotherapeutic agent on the level of cellular apoptotic regulatory proteins in cancer cells of individuals with gastric cancer in order to identify the apoptotic changes.

    Materials & Methods

    This study was a Clinical Trial in which the target group consisted of the patients with gastric cancer who were recognized for the first time and cured under chemotherapy. Thirty-four patients were chosen and categorized randomly into two groups. Case group includes the patients taking PUFAs along with the chemotherapeutic agents. In control group, individuals were under the same chemotherapy protocol without taking PUFAs. Biopsy samples of tumor were taken from the patients before and after chemotherapy. The Bcl-2, Bcl-XL Bid, and Bad gene expression were determined by Real-Time PCR. Also, those proteins upon biopsy samples were surveyed by Frozen Section method.

    Results

    In case group, Bcl-2 and BclXL gene expression and protein levels decreased significantly in comparison with those of the control group. While Bid and Bad gene expression and protein levels increased significantly in comparison with those of the control group.

    Conclusion

    The results of this study showed that use of PUFAs as supplement with Cis-platinum may be useful to stimulate more pro-apoptotic proteins in gastric cancer cells. Consequently, this offers an effective treatment to patients with gastric cancer to respond to chemotherapy.

    Keywords: Pro-apoptotic Proteins, Anti-Apoptotic Proteins, Poly Unsaturated Fatty Acids, Gastric Cancer, Chemoresistance}
  • Elmira Aboutalebi, Ebrahim Sakhinia, Vand Beilanokhi, Homayoun Dolatkhah*
    Background & Aims

     Despite the decline in the prevalence of gastric cancer in recent years, it remains the fourth leading cause of death from cancer in the world. Common cancer treatments may reduce the size of the tumor, but it is transient and does not have a positive effect on the patient's survival and there is a possibility of recurrence of the disease. Strong induction of reticulom endoplasmic has been shown to increase the susceptibility to anti-cancer therapy. Regarding the importance of medicinal herbs in recent years and its low side effects after administration, compared with synthetic drugs, this study investigated the effects of salvia Sclareol purification from sage on the induction of reticulum endoplasmic system stress.

    Materials and Methods

    The MKN-45 cell line from the Pasteur Institute of Iran was purchased and cultured in a complete culture medium of RPMI-1640 with cetacean embryos. Cells cultured with 0, 20, 40, 60, 80 and 100 μm concentrations of Sclareol treatment for 5 hours. The rate of expression of IRE-1 and PERK genes by quantitative real time -PCR and the level of proteins IRE-1 and PERK by western blotting method was investigated.

    Results

    The rate of expression of IRE-1 in doses of 20, 40 and 60 μM Sclareol was significantly increased while decreasing in doses of 80 and 100 μM (p <0.0001). Also, the expression of PERK gene expression at doses of 20, 40 and 60 μM Sclareol was significantly increased, but no increase was observed in doses of 80 and 100 μM (p <0.0001). Also, the levels of IRE-1 and PERK proteins in doses of 20, 40 and 60 micromoles of Sclareol showed a high increase in doses of 80 and 100 μM.

    Conclusion

    From the results of this study, it seems that doses between 20 and 60 μmol of can be Sclareol helpful in increasing the amount of reticuloendoplasmic stress, but doses higher than 60 milimoles do not have like this effect.

    Keywords: gastric Cancer, Sclareol, reticuloendoplasmic system stress}
  • Ali Rezazadeh, Homayun Dolatkhah *, Ahad Mokhtarzadeh, Saeedeh Hozhabr
    Objectives
    Cancer is a hyperactive disorder which can cause uncontrolled propagation of the cells. Several reports indicated that omega polyunsaturated fatty acids can prove their own antitumor effects on different cancerous cells by stopping the operation of the cellular cycle. Therefore, this study mainly aimed to investigate the impact of omega polyunsaturated fatty acids (PUFAs) on the exposition rate of genes CDK1, CyclinB1, and the cellular cycle of the stomach cancerous tissue in under-chemotherapy patients with stomach adenocarcinoma.
    Materials and Methods
    The present study was a double-blind clinical trial in which neither the oncologist nor the patients were aware of the treatment before and after the intervention. The patients with stomach adenocarcinoma were first recognized and subjected to chemotherapy. A total of 24 patients were randomly selected and included in the case and control groups. The patients in the control group were treated with cisplatin and placebo while those of the case group first received cisplatin with the complementary capsule of fatty acids, namely, Natural Factors Ultimate Omega Factors with a dose of 1200 mg and 3600 mg daily, encompassing three 1200 mg medicines each course for 3 weeks. Three samples of the stomach biopsy were taken from all patients before and after the chemotherapy. All mRNA tissues were extracted out of the biopsy samples. Then, DNA was synthesized based on these samples and the exposition rate of the desired genes was measured using the real-time polymerase chain reaction (PCR) method.
    Results
    There was a significant decrease in the mean of exposition of the genes in the case group (P = 0.021) compared to the control group (P = 0.001).
    Conclusions
    Generally, the results revealed that using omega fatty acids 3, 6, and 9 along with cisplatin medicine can be effective in stopping the cell cycle phase G2 in cancerous cells of the stomach tissue.
    Keywords: Stomach adenocarcinoma, PUFAs, G2-M phase of the cellular cycle, Cyclin, cyclin B1, CDK1}
  • Ali Rezazadeh*, Homayun Dolatkhah, Ahad Mokhtarzadeh, Mehran Khojastefard
    Introduction & Objectives

    Gastric cancer is the 5th most common cancer and the third cause of death in the world. Studies have shown that gastric cancer is somewhat susceptible to chemotherapy, but the duration of tumour reduction is short, and patients have not had much success in survival, and in many cases, chemotherapy resistance has been observed. Therefore, the main objective of this study was to investigate the effect of omega-unsaturated fatty acids on the expression of Cyclin A2, and CDK2 germ cell cycle in patients with gastric adenocarcinoma under chemotherapy.

    Materials and Methods

    This is a double-blind, pre-and post-test clinical trial with the target population of patients with gastric adenocarcinoma that were first identified and subjected to chemotherapy. Twenty-four patients were selected randomly and randomly in control and control groups. In the control group, the treatment was routine with cisplatin plus placebo. In the case group, treatment with cisplatin plus a supplement of natural fatty acid supplementation capsules of Ultimate-Omega Factors with a dose of 1200 mg per day was 3,600 mg Three tablets of 1200 mg (for three courses) started on horizons three weeks. Three samples of stomach biopsy were taken from all patients before and after chemotherapy. Biopsy specimens were extracted from all tissue mRNAs and cDNA was synthesized from them, and then the expression of the genes was measured using Real-Time PCR. The results were analyzed by SPSS software version 24.

    Results

    The mean or average expression of Cyclin A2, CDK2 in the case group showed a significant decrease compared to the control group (P value was 0.021 and 0.026, respectively.

    Conclusion

    The results of this study showed that the use of omega-3, 6, 9 fatty acids with cisplatin can be useful in stopping the S-cell cycle in gastric cancer cells.

    Keywords: Gastric Adenocarcinoma, PUFAs, Phase S Cell Cycle, CDK-2, Cyclin A2}
  • MohammadSadra Rasooli, Ali Rezazadeh, Homayun Dolatkhah*
    Background & Aims

    Gastric cancer is the fourth most common cancer and the second cause of death in the world. According to the study, gastric cancer cells have a relative resistance to chemotherapy. Therefore, the purpose of this study was to evaluate the effect of oral administration of omega fatty acids PUFAs) on lipid peroxidation and oxidative stress in gastric cancer in people with gastric cancer before and after chemotherapy.

    Materials & Methods

    This is a double-blind clinical trial. The target group was gastric cancer patients who were first identified and under chemotherapy. Among them, 30 were selected and randomly assigned to two groups. they got. In the control group, the treatment was routine with cisplatin plus placebo. In the case group, treatment with cisplatin plus supplemental capsules of Natural Factors Ultimate-Omega Factors with a dose of 1200 mg per day was 3,600 mg Three tablets of 1200 mg (for three courses) started on horizons three weeks. Three samples of stomach biopsy were taken from all patients before and after chemotherapy. Lipid peroxidation was measured by the Thiobarbituric Acid method and the activity of superoxide dismutase and glutathione peroxidase enzymes by Randox kit. To compare the results, Independent- t-test and Mann-Whitney SPSS software.

    Results

    In the case group, the percentage of lipid peroxidation of the gastric cancer tissue after omega-unsaturated fatty acids increased significantly (P value less than 0.0001). Omega fatty acids caused a significant reduction in the activity of the enzyme superoxide dismutase in the case group was statistically lower than the control group (P value less than 0.0001)

    Conclusion

    The results of this study indicate that the use of omega fatty acids as a complement to cisplatin for controlling gastric cancer can be helpful in increasing the amount of oxidative stress and lipid peroxidation of the gastric cancer tissue in this The study was shown.

    Keywords: Gastric Cancer, PUFAs, Lipids Peroxidation, Oxidative Stress}
  • Seyyed Manuchehr Nourazarian, Mojtaba Ghaffarian, Homayun Dolatkhah*
    Background And Objective
    The relationship between diabetes mellitus and increased risk of cardiovascular diseases has been demonstrated. The aim of this study was to determine the fatty acid profile of epicardial adipose tissue in diabetic and non-diabetic patients with cardiovascular disease.
    Methods
    In this study, 28 diabetic and 40 nondiabetic patients were evaluated. The epicardial adipose tissue and blood samples of patients were collected during surgery. Nonesterified fatty acids and phospholipids were measured by the thin layer chromatography and gas chromatography.
    Results
    Saturated free fatty acids (12: 0) level was higher in diabetic patients compared to nondiabetic patients (P=0.038), while saturated free fatty acids (16: 0) was significantly lower in diabetics (P=0.011). Unsaturated fatty acid (20: 3n-9) was higher in nondiabetics compared to diabetics (P=0.015). There was a significant decrease in level of monounsaturated fatty acids in diabetic patients. The epicardial adipose tissue of diabetics showed a significant increase in free fatty acid (18: 0) and conjugated linoleic acid levels, while there was a significant decrease in the level of free fatty acid (18: 1n-11). Level of epicardial omega-3 free fatty acid (20: 5 n-3) and 22: 6 n -3 was significantly reduced in these patients.
    Conclusion
    Differences in the serum free fatty acid profile of the two groups may be due to differences in their diet, while changes in the fatty acid composition of epicardial adipose tissue in these two groups could be due to impaired metabolism of fatty acids such as uptake, movement and androgen synthesis as a result of diabetes. These changes increase the risk of developing atherosclerosis in diabetic patients.
    Keywords: Diabetes Mellitus, Adipose Tissue, Atherosclerosis, Cardiovascular Disease}
  • احمد موحدیان، شهره علیزاده شرق، سیده زهرا رحمانی، همایون دولتخواه
    زمینه و هدف
    هیپرکلسترولمی فامیلی (Familial Hypercholesterolemia) یک اختلال اتوزومال غالب است که مشخصه آن افزایش مقادیر کلسترول تام و لیپوپروتئین با چگالی پایین (Low Density Lipoprotein) است. فنوتیپ بالینی این بیماری همراه با افزایش خطر بیماری های قلبی-عروقی و مرگ زودهنگام است. جهش های پدید آمده در ژن گیرنده لیپوپروتئین با چگالی پایین (LDLR) می تواند منجر به بروز فنوتیپ FH شود و جهش ژن های دیگر از جمله آپولیپوپروتئین B نیز می تواند همین تابلو را ایجاد کند. از آنجاییکه وراثت و جهش نیز تحت تاثیر عوامل مختلف محیطی از جمله رژیم غذایی و سایر ژن ها واقع می شوند، بنابراین اجرای آزمایشهای روتین برای تعیین سطح کلسترول و LDL بعلت حساسیت بالا و ویژگی پایین، جهت تشخیص زود رس و درمان به موقع کافی نیست. انجام آزمایشات دقیق ملکولی بدلیل حساسیت و ویژگی 100 درصد، برای تعیین جهش های شایع در ژن LDLR (و احتمالا ژن های دیگر) و تعیین دلیل قطعی بیماری، امکان درمان صحیح را تقویت میکند. درحال حاضر روش های PCR-SSCP و Southern-blotting جزو روش های متداول ملکولی برای بررسی اکثر جهش های مهم است. به دلیل تنوع بسیار زیاد نوع جهش در ژن LDLR انجام منطقه ای آزمایشات و تعیین شیوع انواع جهش ها و سپس انجام آزمایشهای روتین برحسب آن نوع جهش ها توصیه می شود.
    کلید واژگان: هیپرکلسترولمی فامیلی, جهش, ژن گیرنده لیپوپروتئین با چگالی کم (LDLR), تشخیص مولکولی}
    Movahedian A., Alizadeh Sharg Sh, Rahmani S. Z, Dolatkhah H
    Background And Objectives
    Familial hypercholesterolemia (FH) is an autosomal disorder characterized by increased levels of total cholesterol and low density lipoprotein cholesterol. The FH clinical phenotype has been associated with increased risk of coronary heart disease and premature death. The mutation in LDLR gene in most cases is responsible for FH phenotype. Furthermore, other gene mutations such as apolipoprotein B- gene may cause similar results. Preliminary research indicates that the FH phenotype is also influenced by other genetic and environmental Factors; therefore, routine clinical analysis such as total cholesterol and LDL-C levels in serum, for early diagnosis and treatment, are not sufficient. Molecular diagnostic investigations, because of high specifity and sensitivity near %100, administered for determining the prevalent mutations in LDLR (and probably other genes) are needed for exact diagnosis and accurate therapy. Currently, PCR-SSCP and southern blotting techniques are among the common techniques that could detect major mutations in gene. Because of wide diversity in kinds of mutations in LDLR gene, we recommend, first, determining the proband's mutation and kinds of mutation, then, performing routine test based on type of mutation.
    Keywords: Familial hyperlipoproteinemia, LDL, R gene molecular diagnosis, mutation, Molecular Diagnostic Method}
فهرست مطالب این نویسنده: 7 عنوان
  • همایون دولتخواه
    دولتخواه، همایون
    (1395) دکتری دکتری تخصصی بیوشیمی بالینی، دانشگاه علوم پزشکی اصفهان
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