Showing 2 results for Farrokhi
Tayebeh Ghanavati, Keyhan Ghatreh-Samani, Effat Farrokhi, Esfandyar Heydarian, Morteza Nikookar,
Volume 25, Issue 129 (10-2015)
Abstract
Background and purpose: Vascular calcification is an important factor in pathogenesis of atherosclerosis. Studies have shown that alkaline phosphatase increases vascular calcification. Here we investigated the effect of gallic acid on alkaline phosphatase gene expression in vascular smooth muscle cells (VSMCs).
Materials and methods: In this experimental study humans aorta VSMCs were incubated with beta glycerol phosphate as calcification-inducing media. Then these cells were treated with 160, 180 and 200 µMol concentration of gallic acid for 24h, 48h and 72h. The total RNA was extracted and cDNA was synthesized and then alkaline phosphatase expression was measured by real time PCR. Alkaline phosphatase specific activity was measured by spectrophotometry.
Results: Overall, 160, 180 and 200 µMol concentration of gallic acid decreased alkaline phosphatase gene expression in vascular smooth muscle cell by 1.98, 2.03, and 3.16 folds, respectively after 72h compared with the control group. The alkaline phosphatase specific activity also decreased compared to that of the control group.
Conclusion: Our results showed that gallic acid decreased the expression and activity of alkaline phosphatase suggesting that this antioxidant compound may attenuate vascular calcification.
Fatemeh Ranjbarnejad, Mozafar Aznab, Kamran Mansouri, Alireza Farrokhi, Tayebeh Ranjbarnejad, Davood Rezazadeh,
Volume 31, Issue 204 (1-2022)
Abstract
This report describes an 89-year-old woman diagnosed with Philadelphia positive Chronic Myeloid Leukemia in 2007 who was initially treated with 200 mg/day imatinib. The patient demonstrated complete molecular response (CMR) in two tests in 2015 and 2018. During treatment between 2007 and 2019, despite increased dosage of imatinib and switching her therapy to nilotinib, complete hematological response was not obtained. ARMS-PCR was performed to find the possible cause of this failed response and JAK2 V617F mutation was detected. The patient with no BCR/ABL1 transcript showed a relatively good molecular response to nilotinib, although the complete hematological response was not observed. According to our findings, tyrosine kinase inhibitor could not be an effective therapy in this JAK2 V617F-positive MPN patient with a BCR/ABL1 mutation.
