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- 저자 : Bahram Masoudi (검색결과 2 건)
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Bahram Masoudi,Mohsen Mardi,Eslam Majidi Hervan,Mohammad Reza Bihamta,Mohammad Reza Naghavi,Babak Nakhoda,Behnam Bakhshi,Mehrzad Ahmadi,Mohammad Taghi Tabatabaei,Mohamad Hossein Dehghani Firouzabadi 한국유전학회 2019 Genes & Genomics Vol.41 No.2
Introduction Some studies in wheat showed that awns may have a useful effect on yield, especially under drought stress. Up to this time few researches has identified the awn length QTLs with different effect in salinity stress. Objective The primary objective of this study was to examine the additive (a) and the epistatic (aa) QTLs involve in wheat awns length in control and saline environments. Methods A F7 RIL population consisting of 319 sister lines, derived from a cross between wheat cultivars Roshan and Falat (seri82), and the two parents were grown in two environments (control and Saline) based on an alpha lattice design with two replications in each environment. At flowering, awn length was measured for each line. For QTL analysis, the linkage map of the ‘‘Roshan × Falat’’ population was used, which included 748 markers including 719 DArT, 29 simple sequenced repeats (SSRs). Additive and pleiotropic QTLs were identified. In order to reveal the relationship between the identified QTL for awns length and the role of the gene or genes that it expresses, the awns length locus location and characteristics of its related CDS, gene, UTRs, ORF, exons and Introns were studied using ensemble plant (http://plant s.ensem bl.org/Triti cum_aesti vum). Furthermore, the promoter analysis has been done using NSITE-PL. Results We identified 6 additive QTLs for awn length by QTL Cartographer program using single-environment phenotypical values. Also, we detected three additive and two epistatic QTLs for awn length by the QTLNetwork program using multienvironment phenotypical values. Our results showed that none of the additive and epistatic QTLs had interactions with environment. One of the additive QTLs located on chromosome 4A was co-located with QTLs for number of sterile spikelet per spike in both environment and number of seed per spike in control environment. Coclusion Studies of the locus linked to the awns length QTL revealed the role of awn and its chloroplasts in grain filing during abiotic stress could be enhanced by over expression of some genes like GTP-Binding proteins which are enriched in chloroplasts encoded by genes included wPt-5730 locus.
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Nastaran Masoudi Khoram,Bahareh Bigdeli,Alireza Nikoofar,Bahram Goliaei 한국유방암학회 2016 Journal of breast cancer Vol.19 No.1
Purpose: Breast cancer is an important cause of death among women. The development of radioresistance in breast cancer leads to recurrence after radiotherapy. Caffeic acid phenethyl ester (CAPE), a polyphenolic compound of honeybee propolis, is known to have anticancer properties. In this study, we examined whether CAPE enhanced the radiation sensitivity of MDAMB- 231 (estrogen receptor-negative) and T47D (estrogen receptor- positive) cell lines. Methods: The cytotoxic effect of CAPE on MDA-MB-231 and T47D breast cancer cells was evaluated by performing an 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay. To assess clonogenic ability, MDAMB- 231 and T47D cells were treated with CAPE (1 μM) for 72 hours before irradiation, and then, a colony assay was performed. A comet assay was used to determine the number of DNA strand breaks at four different times. Results: CAPE decreased the viability of both cell lines in a dose- and time-dependent manner. In the clonogenic assay, pretreatment of cells with CAPE before irradiation significantly reduced the surviving fraction of MDA-MB-231 cells at doses of 6 and 8 Gy. A reduction in the surviving fraction of T47D cells was observed relative to MDA-MB-231 at lower doses of radiation. Additionally, CAPE maintained radiation-induced DNA damage in T47D cells for a longer period than in MDA-MB-231 cells. Conclusion: Our results indicate that CAPE impairs DNA damage repair immediately after irradiation. The induction of radiosensitivity by CAPE in radioresistant breast cancer cells may be caused by prolonged DNA damage.
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