977 resultados para 182-1133C
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利用~(152)Sm(~(35)Cl,5nγ)~(182)Au核反应产生并研究了双奇核~(182)Au的高自旋态,首次建立了双奇核~(182)Au基于πh_(9/2)(×)Vi(13/2)和πi_(13/2)(×)Vi_(13/2)准粒子组态上的转动带能级纲图,发现在低自旋区,两个转动带能级均出现旋称反转.用推转壳模型对~(182)Au的转动带能级进行了理论研究,发现当采用形变和对力自洽计算后,从理论上可以定性地解释~(182)Au核中两个转动带出现的旋称反转现象。
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Search for low-spin signature inversion in the pi i(13/2) circle times nu i(13/2) bands in odd-odd Au-182,Au-184,Au-186 has been conducted through the standard in-beam gamma-spectroscopy techniques. The experiments for Au-182 and 186Au have been performed in the Japan Atomic Energy Agency (JAEA) via the Sm-152(Cl-35,5n)Au-182 and Yb-172(F-19,5n)Au-186 reactions, respectively. A study of Au-184 has been made using a multi-detector array GASP in LNL, Italy, via the Tb-159(Si-29,4n)Au-184 reaction. The pi i(13/2) circle times nu i(13/2) bands in these three nuclei have been identified and extended up to high-spin states. In particular, the inter-band connection between the pi i(13/2) nu i(13/2) band and the ground-state band in 184 Au has been established, leading to a firm spin-and-parity assignment for the pi i(13/2) circle times nu i(13/2) band. The low-spin signature inversion is found in the pi i(13/2) circle times nu i(13/2) bands in Au-182,Au-184,Au-186 according to our spin-assignment and the signature crossing observed at high-spin states.
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Search for low-spin signature inversion in the pi i(13/2) circle times nu i(13/2) bands in odd-odd Au-182,Au-184,Au-186 has been conducted through the standard in-beam gamma-spectroscopy techniques via the Sm-152(Cl-35,5n) Au-182, Yb-172(F-19,5n) (186)An, and Tb-159(Si-29,4n) (184)An reactions, respectively. The pi i(13/2) circle times nu i(13/2) bands in these three nuclei have been identified and extended up to high-spin states. In particular, the inter-band connection between the pi i(13/2) circle times nu i(13/2) band and the ground-state band in Au-184 has been established, leading to a firm spin-and-parity assignment for the pi i(13/2) circle times nu i(13/2) band. The low-spin signature inversion is found in the pi i(13/2) circle times nu i(13/2) bands according to our spin-assignment and-the signature crossing observed at high-spin states.
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36 fotografías a color.
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Splenic marginal zone lymphoma (SMZL) is a low grade B-cell non-Hodgkin's lymphoma. The molecular pathology of this entity remains poorly understood. To characterise this lymphoma at the molecular level, we performed an integrated analysis of 1) genome wide genetic copy number alterations 2) gene expression profiles and 3) epigenetic DNA methylation profiles.We have previously shown that SMZL is characterised by recurrent alterations of chromosomes 7q, 6q, 3q, 9q and 18; however, gene resolution oligonucleotide array comparative genomic hybridisation did not reveal evidence of cryptic amplification or deletion in these regions. The most frequently lost 7q32 region contains a cluster of miRNAs. qRT-PCR revealed that three of these (miR-182/96/183) show underexpression in SMZL, and miR-182 is somatically mutated in >20% of cases of SMZL, as well as in >20% of cases of follicular lymphoma, and between 5-15% of cases of chronic lymphocytic leukaemia, MALT-lymphoma and hairy cell leukaemia. We conclude that miR-182 is a strong candidate novel tumour suppressor miRNA in lymphoma.The overall gene expression signature of SMZL was found to be strongly distinct fromthose of other lymphomas. Functional analysis of gene expression data revealed SMZL to be characterised by abnormalities in B-cell receptor signalling (especially through the CD19/21-PI3K/AKT pathway) and apoptotic pathways. In addition, genes involved in the response to viral infection appeared upregulated. SMZL shows a unique epigenetic profile, but analysis of differentially methylated genes showed few with methylation related transcriptional deregulation, suggesting that DNA methylation abnormalities are not a critical component of the SMZL malignant phenotype.
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Light brown sediment with clasts ranging from small to medium in size. The clast shape ranges from sub-angular to sub-rounded. Rotation structures can commonly be seen, along with some comet structures as well. A few lineations and edge-to-edge grain crushing can also be observed. There is also the inclusion of a fine grained domain that is a darker brown (tanned-brown).
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Light brown sediment with clasts ranging from small to medium in size. Clast shape ranges from angular to sub-rounded. Rotation structures are abundant throughout the sample. Comet structures and lineations can also be seen.
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L’objectif de cette étude consiste à déterminer si les conventions de l’Organisation internationale du travail (OIT) sont effectives en ce qui concerne l’éradication du travail des enfants en Mauritanie. Cette effectivité est appréciée en mesurant la réception juridique et la réception sociale en Mauritanie de la Convention 29 sur le travail forcé, de la Convention 138 sur l’âge minimum d’admission à l’emploi et de la Convention 182 sur les pires formes de travail des enfants. La réception juridique des conventions est mesurée par un examen de l’intégration de leurs dispositions dans le droit national mauritanien. La réception juridique comprend également l’appréciation du contrôle du respect des conventions en territoire mauritanien. La réception sociale fait référence, quant à elle, aux stratégies de mise en œuvre des conventions de l’OIT par le Gouvernement mauritanien à travers ses programmes et ses politiques. Notre analyse démontre que l’effectivité des Conventions 29, 138 et 182 de l’OIT en ce qui concerne l’éradication du travail des enfants en Mauritanie est, selon nous, partielle. Dans l’ensemble, la situation tend à s’améliorer et le Gouvernement mauritanien tente de respecter l’esprit de ces conventions et de leur faire écho dans le droit national. Toutefois, il n’existe pas beaucoup d’information sur l’impact des programmes mis en place pour éradiquer le travail des enfants.
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Cell culture models of antioestrogen resistance often involve applying selective pressures of oestrogen deprivation simultaneously with addition of tamoxifen or fulvestrant (Faslodex, ICI 182,780) which makes it difficult to distinguish events in development of antioestrogen resistance from those in loss of response to oestrogen or other components. We describe here time courses of loss of antioestrogen response using either oestrogen-maintained or oestrogen-deprived MCF7 cells in which the only alteration to the culture medium was addition of 10(-6) M tamoxifen or 10(-7) M fulvestrant. In both oestrogen-maintained and oestrogen-deprived models, loss of growth response to tamoxifen was not associated with loss of response to fulvestrant. However, loss of growth response to fulvestrant was associated in both models with concomitant loss of growth response to tamoxifen. Measurement of oestrogen receptor alpha (ER alpha) and oestrogen receptor beta (ER beta) mRNA by real-time RT-PCR together with ER alpha and ER beta protein by Western immunoblotting revealed substantial changes to ER alpha levels but very little alteration to ER beta levels following development of antioestrogen resistance. In oestrogen-maintained cells, tamoxifen resistance was associated with raised levels of ERa mRNA/protein. However by contrast, in oestrogen-deprived MCF7 cells, where oestrogen deprivation alone had already resulted in increased levels of ERa mRNA/protein, long-term tamoxifen exposure now reduced ER alpha levels. Whilst long-term exposure to fulvestrant reduced ERa. mRNA/protein levels in the oestrogen-maintained cells to a level barely detectable by Western immunoblotting and non-functional in inducing gene expression (ERE-LUC reporter or pS2), in oestrogen-deprived cells the reduction was much less substantial and these cells retained an oestrogen-induction of both the ERE-LUC reporter gene and the endogenous pS2 gene which could still be inhibited by antioestrogen. This demonstrates that whilst ER alpha can be abrogated by fulvestrant and increased by tamoxifen in some circumstances, this does not always hold true and mechanisms other than alteration to ER must be involved in the development of antioestrogen resistant growth. (c) 2006 Elsevier Ltd. All rights reserved.