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- Ablikim, M., et al.
(författare)
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Measurements of (XcJ)-> K+K-K+K- decays
- 2006
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 642:3, s. 197-202
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Tidskriftsartikel (refereegranskat)abstract
- Using 14M psi(2S) events taken with the BESII detector, chi(cJ) -> 2(K+K-) decays are studied. For the four-kaon final state, the branching fractions are B(chi(c0,1,2) ->.2(K+K-)) = (3.48 +/- 0.23 +/- 0.47) x 10(-3), (0.70 +/- 0.13 +/- 0.10) x 10(-3), and (2.17 +/- 0.20 +/- 0.31) x 10(-3). For the phi K+K- final state, the branching fractions, which are measured for the first time, are B(chi(c0,1,2) -> phi K+K-) = (1.03 +/- 0.22 +/- 0.15) x 10(-3), (0.46 +/- 0.16 +/- 0.06) x 10(-3), and (1.67 +/- 0.26 +/- 0.24) x 10(-4). For the phi phi final state, B(chi(c0,2) -> phi phi) = (0.94 +/- 0.21 +/- 0.13) x 10(-3) and (1.70 +/- 0.30 +/- 0.25) x 10(-3).
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| 2. |
- Abazov, V. M., et al.
(författare)
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The upgraded DO detector
- 2006
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Ingår i: Nuclear Instruments and Methods in Physics Research Section A. - : Elsevier BV. - 0168-9002 .- 1872-9576. ; 565:2, s. 463-537
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Tidskriftsartikel (refereegranskat)abstract
- The DO experiment enjoyed a very successful data-collection run at the Fermilab Tevatron collider between 1992 and 1996. Since then, the detector has been upgraded to take advantage of improvements to the Tevatron and to enhance its physics capabilities. We describe the new elements of the detector, including the silicon microstrip tracker, central fiber tracker, solenoidal magnet, preshower detectors, forward muon detector, and forward proton detector. The uranium/liquid -argon calorimeters and central muon detector, remaining from Run 1, are discussed briefly. We also present the associated electronics, triggering, and data acquisition systems, along with the design and implementation of software specific to DO.
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| 3. |
- Artner, Isabella, et al.
(författare)
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MaFA is a dedicated activator of the insulin gene in vivo.
- 2008
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Ingår i: Journal of Endocrinology. - 1479-6805. ; May 30, s. 271-279
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Tidskriftsartikel (refereegranskat)abstract
- As successful generation of insulin producing cells could be used for diabetes treatment, a concerted effort is being made to understand the molecular programs underlying islet beta cell formation and function. The closely related MafA and MafB transcription factors are both key mammalian beta cell regulators. MafA and MafB are co-expressed in insulin+ beta cells during embryogenesis, while in the adult pancreas MafA is only produced in beta cells and MafB in glucagon+ alpha cells. MafB-/- animals are also deficient in insulin+ and glucagon+ cell production during embryogenesis. However, only MafA over-expression selectively induced endogenous Insulin mRNA production in cell line based assays, while MafB specifically promoted Glucagon expression. Here we analyzed if these factors were sufficient to induce insulin+ and/or glucagon+ cell formation within embryonic endoderm using the chick in ovo electroporation assay. Ectopic expression of MafA, but not MafB, promoted Insulin production, however neither MafA nor MafB were capable of inducing Glucagon. Co-electroporation of MafA with the Ngn3 transcription factor resulted in the development of more organized cell clusters containing both insulin and glucagon producing cells. Analysis of chimeric proteins of MafA and MafB demonstrated that chick Insulin activation depended on sequences within the MafA C-terminal DNA binding domain. MafA was also bound to Insulin and Glucagon transcriptional control sequences in mouse embryonic pancreas and beta cell lines. Collectively, these results demonstrate a unique ability for MafA to independently activate Insulin transcription.
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| 4. |
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| 5. |
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| 6. |
- Wang, Ming-Wei, et al.
(författare)
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Expression of PINCH protein in gliomas and its clinicopathological significance
- 2007
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Ingår i: Oncology. - : S. Karger AG. - 0890-9091 .- 0030-2414 .- 1423-0232. ; 72:5-6, s. 343-346
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: Particularly interesting new cysteine-histidine-rich protein (PINCH), as a LIM domain adapter protein, functions in the integrin and growth factor signal transduction pathway, and is upregulated in tumor-associated stroma in several types of cancers. However, no study of PINCH has been carried out in gliomas, therefore we examined PINCH expression in gliomas and its clinicopathological significance. Methods: PINCH expression was immunohistochemically examined in 82 gliomas, along with 26 matched adjacent normal brain samples and 10 recurred gliomas. Results: PINCH was strongly expressed in the primary (35%, p = 0.0001) or recurred tumors (40%, p = 0.004) and weak in normal brain tissue. PINCH expression was significantly increased in high-grade gliomas (55 vs. 24%, high- vs. low-grade gliomas, p = 0.004). There was no association of PINCH expression with gender, age, tumor number, size, histological type and tumor location (p > 0.05). Conclusions: PINCH expression may be involved in glioma development and differentiation. Copyright © 2008 S. Karger AG.
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| 7. |
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| 8. |
- Zhang, Jin-Ting, et al.
(författare)
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Nuclear to cytoplasmic shift of p33ING1b protein from normal oral mucosa to oral squamous cell carcinoma in relation to clinicopathological variables
- 2008
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Ingår i: Journal of Cancer Research and Clinical Oncology. - : Springer Science and Business Media LLC. - 0171-5216 .- 1432-1335. ; 134:3, s. 421-426
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: p33ING1b, as a candidate tumour suppressor gene, has been found to be expressed a proportion of oral squamous cell carcinomas (OSCCs), however, its clinicopathological significance is not studied yet. Our aim was to investigate association of p33ING1b expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in OSCCs. Methods: p33ING1b expression was immumohistochemically examined in 20 normal oral mucosa specimens and 49 OSCCs. Results: Normal squamous cells showed only p33ING1b nuclear expression (no cytoplasmic expression), with a rate of 90% positive cases. While 24% of OSCCs appeared cytoplasmic expression (11 of them with weak nuclear staining) and the rest tumours (76%) were negative for p33 ING1b. Furthermore, the cases having lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P = 0.03). The p33ING1b cytoplasmic expression was positively related to PINCH expression (P = 0.04), the cases positive for both proteins had a high rate of the metastasis (P = 0.03). Conclusions: The transfer of p33ING1b protein from the nucleus to the cytoplasm may result in loss of normal cellular function of the protein, which might play a role in the tumourigenesis and metastasis of OSCCs. © 2007 Springer-Verlag.
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