| 1. |
- Abdesselam, A., et al.
(författare)
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The ATLAS semiconductor tracker end-cap module
- 2007
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Ingår i: Nuclear Instruments and Methods in Physics Research Section A. - : Elsevier BV. - 0168-9002 .- 1872-9576. ; 575:3, s. 353-389
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Tidskriftsartikel (refereegranskat)abstract
- The challenges for the tracking detector systems at the LHC are unprecedented in terms of the number of channels, the required read-out speed and the expected radiation levels. The ATLAS Semiconductor Tracker. (SCT) end-caps have a total of about 3 million electronics channels each reading out every 25 ns into its own on-chip 3.3 mu s buffer. The highest anticipated dose after 10 years operation is 1.4x10(14) cm(-2) in units of 1 MeV neutron equivalent (assuming the damage factors scale with the non-ionising energy loss). The forward tracker has 1976 double-sided modules, mostly of area similar to 70 cm(2), each having 2 x 768 strips read out by six ASICs per side. The requirement to achieve an average perpendicular radiation length of 1.5% X-0, while coping with up to 7 W dissipation per module (after irradiation), leads to stringent constraints on the thermal design. The additional requirement of 1500e(-) equivalent noise charge (ENC) rising to only 1800e(-) ENC after irradiation, provides stringent design constraints on both the high-density Cu/Polyimide flex read-out circuit and the ABCD3TA read-out ASICs. Finally, the accuracy of module assembly must not compromise the 16 mu m (r phi) resolution perpendicular to the strip directions or 580 mu m radial resolution coming from the 40 mrad front-back stereo angle. A total of 2210 modules were built to the tight tolerances and specifications required for the SCT. This was 234 more than the 1976 required and represents a yield of 93%. The component flow was at times tight, but the module production rate of 40-50 per week was maintained despite this. The distributed production was not found to be a major logistical problem and it allowed additional flexibility to take advantage of where the effort was available, including any spare capacity, for building the end-cap modules. The collaboration that produced the ATLAS SCT end-cap modules kept in close contact at all times so that the effects of shortages or stoppages at different sites could be rapidly resolved.
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| 2. |
- Mostovich, Luydmila A, et al.
(författare)
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Integrin alpha9 (ITGA9) expression and epigenetic silencing in human breast tumors
- 2011
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Ingår i: CELL ADHESION and MIGRATION. - : Landes Bioscience. - 1933-6918 .- 1933-6926. ; 5:5, s. 395-401
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Tidskriftsartikel (refereegranskat)abstract
- Integrin alpha9 (ITGA9) is one of the less studied integrin subunits that facilitates accelerated cell migration and regulates diverse biological functions such as angiogenesis, lymphangiogenesis, cancer cell proliferation and migration. In this work, integrin alpha9 expression and its epigenetic regulation in normal human breast tissue, primary breast tumors and breast cancer cell line MCF7 were studied. It was shown that integrin alpha9 is expressed in normal human breast tissue. In breast cancer, ITGA9 expression was downregulated or lost in 44% of tumors while another 45% of tumors showed normal or increased ITGA9 expression level (possible aberrations in the ITGA9 mRNA structure were supposed in 11% of tumors). Methylation of ITGA9 CpG-island located in the first intron of the gene was shown in 90% of the breast tumors with the decreased ITGA9 expression while no methylation at 5-untranslated region of ITGA9 was observed. 5-aza-dC treatment restored integrin alpha9 expression in ITGA9-negative MCF7 breast carcinoma cells, Trichostatin A treatment did not influenced it but a combined treatment of the cells with 5-aza-dC/Trichostatin A doubled the ITGA9 activation. The obtained results suggest CpG methylation as a major mechanism of integrin alpha9 inactivation in breast cancer with a possible involvement of other yet unidentified molecular pathways.
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| 3. |
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| 4. |
- Mostovich, Luydmila A, et al.
(författare)
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The TCF4/beta-catenin pathway and chromatin structure cooperate to regulate D-glucuronyl C5-epimerase expression in breast cancer
- 2012
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Ingår i: Epigenetics. - : Landes Bioscience. - 1559-2294 .- 1559-2308. ; 7:8, s. 930-939
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Tidskriftsartikel (refereegranskat)abstract
- D-glucuronyl C5-epimerase (GLCE) is a potential tumor-suppressor gene involved in heparan sulfate biosynthesis. GLCE expression is significantly decreased in breast tumors; however, the underlying molecular mechanisms remain unclear. This study examined the possible epigenetic mechanisms for GLCE inactivation in breast cancer. Very little methylation of the GLCE promoter region was detected in breast tumors in vivo and in breast cancer cells (MCF7 and T47D) in vitro and GLCE expression in breast cancer cells was not altered by 5-deoxyazacytidine (5-aza-dC) treatment, suggesting that promoter methylation is not involved in regulating GLCE expression. Chromatin activation by Trichostatin A (TSA) or 5-aza-dC/TSA treatment increased GLCE expression by two to 3-fold due to an increased interaction between the GLCE promoter and the TCF4/beta-catenin transactivation complex, or H3K9ac and H3K4Me3 histone modifications. However, ectopic expression of TCF4/beta-catenin was not sufficient to activate GLCE expression in MCF7 cells, suggesting that chromatin structure plays a key role in GLCE regulation. Although TSA treatment significantly repressed canonical WNT signaling in MCF7 cells, it did not influence endogenous TCF4/beta-catenin mRNA levels and activated TCF4/beta-catenin-driven transcription from the GLCE promoter, indicating GLCE as a novel target for TCF4/beta-catenin complex in breast cancer cells. A correlation was observed between GLCE, TCF4 and beta-catenin expression in breast cancer cells and primary tumors, suggesting an important role for TCF4/beta-catenin in regulating GLCE expression both in vitro and in vivo. Taken together, the results indicate that GLCE expression in breast cancer is regulated by a combination of chromatin structure and TCF4/beta-catenin complex activity.
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| 5. |
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| 6. |
- Evgenieva, Tsvetina, et al.
(författare)
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Three-point observation in the troposphere over Sofia-Plana Mountain,Bulgaria
- 2011
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Ingår i: International Journal of Remote Sensing. - : Informa UK Limited. - 0143-1161 .- 1366-5901. ; 32:24, s. 9343-9363
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Tidskriftsartikel (refereegranskat)abstract
- Based on a novel combination of approaches and instruments, this article presents campaign-based results from atmospheric boundary layer (ABL) height and aerosol optical depth (AOD) measurements carried out at two different experimental sites in Sofia, as well as from three-point measurements of aerosol number concentrations. Several instruments (lidar (developed by the IE), ceilometer, aerosol particle counter, sun photometer and meteorological sensors) were used in this study. Based on joint interpretation of the instruments' data we assess the influence of the atmospheric aerosol in the planetary boundary layer and the significant influence of aerosol layers and high clouds on AOD values. Measurements of AOD in the city basin gave values in the range 0.22-0.41 for cloud-free skies, and up to around 0.8 under partly cloudy conditions. The information obtained during the two campaigns indicates that aerosol particle concentrations were lower in park areas than along heavy-traffic thoroughfares in the city, but higher than in the mountain area. In conclusion, our study demonstrates the potential of employing a broad array of instruments for the study of boundary layer and aerosol over large, valley-situated and heavily urbanized city areas.
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| 11. |
- Prudnikova, Tatiana Y, et al.
(författare)
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miRNA-218 contributes to the regulation of D-glucuronyl C5-epimerase expression in normal and tumor breast tissues
- 2012
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Ingår i: Epigenetics. - : Landes Bioscience. - 1559-2294 .- 1559-2308. ; 7:10, s. 1109-1114
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Tidskriftsartikel (refereegranskat)abstract
- microRNAs (miRNAs) are key posttranscriptional regulators of gene expression. In the present study, regulation of tumor-suppressor gene D-glucuronyl C5-epimerase (GLCE) by miRNA-218 was investigated. Significant downregulation of miRNA-218 expression was shown in primary breast tumors. Exogenous miRNA-218/anti-miRNA-218 did not affect GLCE mRNA but regulated GLCE protein level in MCF7 breast carcinoma cells in vitro. Comparative analysis showed a positive correlation between miRNA-218 and GLCE mRNA, and negative correlation between miRNA-218 and GLCE protein levels in breast tissues and primary tumors in vivo, supporting a direct involvement of miRNA-218 in posttranscriptional regulation of GLCE in human breast tissue. A common scheme for the regulation of GLCE expression in normal and tumor breast tissues is suggested.
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