Elemental analysis of Egyptian crude oils by INAA using rabbit irradiation system at ETRR-2 reactor

Instrumental neutron activation analysis (INAA) using rabbit irradiation system at ETRR-2 reactor was utilized to analyze some elements namely Na, Mg, Al, Cl, V, Mn, In, and Br in four different crude petroleum samples from different oil fields in the Suez-Gulf region of Egypt. The INAA was performed by four different standardization methods. Namely absolute, single comparator based on effective cross section concept, single comparator based on k_0,Au factors, and that based on k_0,ic factors defined versus any suitable internal comparator method. A FORTRAN computer program was written to calculate the extracted concentrations by these methods. A reasonable agreement between the obtained results was noticed.     

骨髓间质干细胞吲哚胺2，3-双加氧酶活性对T淋巴细胞的影响(英文)

目的: 探讨骨髓间质干细胞（MSCs）吲哚胺2，3-双加氧酶（IDO）活性对抑制T淋巴细胞应答反应的影响。方法: 从人骨髓中分离培养间质干细胞,通过其形态特点、表面标志及多向分化能力检测进行鉴定。以浓度为2×105 U/L的 IFN-γ对分离的MSCs诱导18 h，检测MSCs上IDO mRNA和IDO蛋白表达。将经过IFN-γ 2×105 U/L诱导的MSCs预先接种在培养板中，再建立混合淋巴细胞培养(MLR)体系，利用MTT法检测T淋巴细胞增殖率，并用反相高效液相色谱法检测IDO活性。结果: IFN-γ能诱导MSCs上IDO mRNA和IDO蛋白的表达；MSCs的IDO活性抑制MLR体系中T淋巴细胞增殖率。结论： 经IFN-γ刺激后的MSCs在体外可抑制异体T淋巴细胞的免疫应答，IDO活性参与了这种免疫抑制作用的发挥。     

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??WANG Yan*??YU Jie??LI Xiao-jing??ZHOU Min??HUANG Cheng??WANG Xue-mei.* Key Laboratory of Child Development and Disorders Cofounded by Chongqing and Ministry of Education ??Chongqing Key Laboratory of Pediatrics??Chongqing International Science and Technology Cooperation Center for Child Development and Disorders??Children’s Hospital of Chongqing Medical University??Chongqing 400014??China
Objective To explore the inhibition effect of Tanshinone IIA on the activation of nuclear factor-kappa B ??NF-κB?? and the expression of TNF-α??IL-8 in peripheral blood mononuclear cells ??PBMC?? of the acute phase of Kawasaki disease??KD?? and to explore the pathogenesis of KD and to explore the anti-inflammatory effect of Tanshinone IIA. Methods PBMCs were isolated and purified from peripheral blood of 20 KD children and 20 healthy children by density gradient centrifugation. In every sample PBMC were divided into five groups.The first group was cultured naturally?? the second one was stimulated by phorbol 12-myristate-13-acetate ??PMA????while other groups were stimulated by PMA and TanshinoneIIA which was treated with different concentrations.Each group was cultured in carbon dioxide incubator. Activation of NF-κB in PBMCs was determined by immunocytochemistry?? and ELISA was used to measure the concentration of TNF-α??IL-8 in supernatant. Results Under PMA culturing?? the activation of NF-κB was significantly higher than the blank group both in KD and control group??P??0.05???? in supernatant of the two?? the expression of TNF-α??IL-8 was significantly higher than the blank group??P??0.05??P??0.01??.Under PMA+ final concentration of 3mg / l Tan II A culturing?? the activation of NF-κB in KD and control group was significantly lower than the PMA group??P??0.05???? the expression of IL-8 in KD and control group and the expression of TNF-α in KD group were significantly lower than the PMA group??P??0.05????while the control group??concerning of TNF-α?? there was no significant decline??P??0.05??. Under PMA+ final concentration of 10mg / l Tan II A culturing?? the activation of NF-κB in KD and control group was significantly lower than the PMA group??P??0.05???? in supernatant of the KD and control group the expression of TNF-α and IL-8 was significantly lower too?? and the PMA+ final concentration of 10mg / l Tan II A group was lower than the PMA+ final concentration of 3mg / l Tan II A group??P??0.05?? both in the KD and control group. There was obvious positive correlation between the activation of NF-κB in PBMCs and the expression of TNF-α??IL-8 in the cultured supernatant??r = 0.817??r = 0.782??P??0.01????and there was also obvious positive correlation between the expression of TNF-α and IL-8??r = 0.709?? P??0.01??.Conclusion The activation of NF-κB is enhanced and the expression of TNF-α??IL-8 is increased in PBMC of the acute phase of Kawasaki disease??which may be involved in immune inflammatory response and may mediate immune vasacular injury. The anti-inflammatory mechanism of TanshinoneIIA in PBMC of the acute phase of Kawasaki disease may inhibit the activation of NF-κB and the subsequent expression of TNF-α and IL-8??and this anti-inflammatory effect has a dose-dependence     

小鼠胚胎心脏发育过程中胰岛素基因增强子结合蛋白1的时序表达与组蛋白乙酰化酶p300的关系

目的观察小鼠胚胎心脏发育过程中转录因子胰岛素基因增强子结合蛋白1(Islet-1)的时序性表达规律,并探讨其与组蛋白乙酰化酶p300介导的组蛋白乙酰化调控网络中的关系。方法以健康6～8周龄昆明小鼠为研究对象,下午1700雄雌按12比例合笼,次日观察阴栓,观察到阴栓最早之日计为胎龄0.5 d(E0.5)。取胎龄为E11.5、E14.5、E17.5的胎鼠和新生鼠的心脏,利用Western blot方法定量分析Islet-1的时序性表达规律,并利用蛋白质免疫共沉淀(Co-IP)和串联质谱分析方法(MS)鉴定Islet-1与组蛋白乙酰化酶p300的关系,同时应用Western blot方法反验证实验结果。结果 1.在小鼠胚胎心脏发育过程中,Islet-1在E14.5时的表达水平(0.434±0.353)明显高于与其在E11.5(0.074±0.456)、E17.5(0.120±0.127)和新生鼠(0.049±0.083)的表达水平,差异均有统计学意义(Pa<0.05),而其他时间点(E11.5、E17.5和新生鼠)间的表达差异无统计学意义(Pa>0.05)。2.在胚胎心脏发育过程中,Islet-1与组蛋白乙酰化酶p300相互结合,以蛋白复合物的形式存在。结论在小鼠胚胎心脏发育过程中,Islet-1可能作为枢纽因子,募集组蛋白乙酰化酶p300参与组蛋白乙酰化修饰调控。     

Overexpression of IL-8 promotes cell migration via PI3K-Akt signaling pathway and EMT in triple-negative breast cancer

Triple-negative breast cancer (TNBC) is a type of malignant and heterogeneous tumor in premenopausal females with ineffective therapeutic targets. IL-8 is one of the earliest discovered chemotaxis cytokines which expression is closely related to the progress of various cancers. Previous studies showed that IL-8 determines the prognosis of TNBC patients, nevertheless how IL-8 influences the progress of TNBC is unclear. In our studies, we discovered that overexpression of IL-8 promotes TNBC cells (TNBCs) migration and tumor growth via the PI3K-Akt and MAPK signaling pathway. Cell-cycle of TNBCs arrest at S phase by overexpression of IL-8, however, there is no significant variation on the cell viability and cell apoptosis of TNBCs. Besides, overexpression of IL-8 result in the downregulation of E-cadherin and the upregulation of Cyclin B1 in MDA-MB-231 cells. Taken together, our results suggest that IL-8 performs a crucial role in the progress of TNBC, and it could be a novel therapeutic target of TNBC.