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5篇 您的检索式:作者名="O.I"
    题名 作者 年代 出处 被引量
1查看详情显示文摘Lulevich V.V Nordschild S Vinogradova O.I 0,,:1
2查看详情显示文摘El-Sabbagh O.I Baraka M.M Ibrahim S.M Pannecouque P Andrei G Snoeck R Balzarini J Rashad A.A 0,,:1
3Aircraft noise modelling for environmental assessment around airports显示文摘Zaporozhets O.I Tokarev V.I 0,,02:1
4Statistical Properties of The Exponentiated Nakagami Distribution显示文摘Adepoju K.A Chukwu A.U and Shittu, O.I 2014Journal of Mathematics and System Science2014,4,3:0
5Phosphorylation of Protein Kinase Akt by Mtorc2 in Peripheral Blood Mononuclear Cells of Patients with Cancer and Diabetes显示文摘Akt/mTOR/p70S6K1 signaling pathway plays an important role in the pathogenesis of cancer and diabetes.Macrophages and lymphocytes are involved in the pathogenesis of diabetes,diabetic atherosclerosis,formation of insulin resistance as well as immune response to cancer and tumor maintenance.The aim of the study was to determine the Akt activation by mTORC2 in peripheral blood mononuclear cell(PBMC)of patients with type 2 diabetes and cancer.The following groups were studied:control group,patients with type 2 diabetes,cancer patients and patients with both cancer and diabetes.The amounts of phospho-Akt(р-S473)and phospho-p70S6K1(p-T389)were determined using ELISA kits.The amount of phosphorylated Akt significantly increases in PBMC of patients with cancer.There was no effect in PBMC from patients with type 2 diabetes and significant decrease in the amount of phospho-Akt in PBMC of the patients group both with cancer and diabetes.p70S6K1 activation was observed in PBMC of the groups 2 and 3 patients.Thus,chronic diseases such as type 2 diabetes and cancer can affect the signaling mechanisms in blood cells.The state of Akt phosphorylation in leukocytes can indicate the activity of mTORC1 and its substrates,which may be important for the evaluation of the pathological process and the efficacy of the drugs.Vatseba T.S Sokolova L.K Pushkarev V.V Kovzun O.I Pushkarev V.M Guda B.B Tronko M.D 2019Journal of Endocrinology Research2019,1,1:0
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