| 1. |
- Weinstein, John N., et al.
(författare)
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The cancer genome atlas pan-cancer analysis project
- 2013
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 45:10, s. 1113-1120
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Forskningsöversikt (refereegranskat)abstract
- The Cancer Genome Atlas (TCGA) Research Network has profiled and analyzed large numbers of human tumors to discover molecular aberrations at the DNA, RNA, protein and epigenetic levels. The resulting rich data provide a major opportunity to develop an integrated picture of commonalities, differences and emergent themes across tumor lineages. The Pan-Cancer initiative compares the first 12 tumor types profiled by TCGA. Analysis of the molecular aberrations and their functional roles across tumor types will teach us how to extend therapies effective in one cancer type to others with a similar genomic profile. © 2013 Nature America, Inc. All rights reserved.
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| 2. |
- Chen, DeJiu, et al.
(författare)
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DySCAS System Architecture
- 2007
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Rapport (refereegranskat)abstract
- This deliverable provides an architectural strategy and overall system design forthe DySCAS middleware system as a first step towards a complete systemspecification. The DySCAS Basic Architecture captures both the systemconceptualization and an initial function-level outline without consideringimplementation and technology details. It defines the middleware system in termsof its application and operational contexts, expected features, middleware servicesthat group functions, behaviours, as well as the structuring and implementationdecisions that are most crucial to satisfy the given set of requirements. In thisdocument, we also outline some fundamental strategies for binding themiddleware components to the target platforms and infrastructures and forhandling potential errors at both initialization-time and rum-time, while taking thetechnology support and domain needs into consideration.This deliverable also covers the rationale behind the architecture solutions andprovides a generic framework that relates architecture principles and styles, wellknownmechanisms, and reference models to the expected functionalities andqualities of DySCAS. The aim is to consolidate the proposed solutions and also tofacilitate the communications between DySCAS partners and to third-parties.
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| 4. |
- Törnudd, Mattias, et al.
(författare)
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Protamine stimulates platelet aggregation in vitro with activation of the fibrinogen receptor and alpha-granule release, but impairs secondary activation via ADP and thrombin receptors
- 2021
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Ingår i: Platelets. - : Taylor & Francis. - 0953-7104 .- 1369-1635. ; 32:1, s. 90-96
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Tidskriftsartikel (refereegranskat)abstract
- Heparin and protamine are fundamental in the management of anticoagulation during cardiac surgery. Excess protamine has been associated with increased bleeding. Interaction between protamine and platelet function has been demonstrated but the mechanism remains unclear. We examined the effect of protamine on platelet function in vitro using impedance aggregometry, flow cytometry, and thrombin generation. Platelets were exposed to protamine at final concentrations of 0, 20, 40, and 80 mu g/mL, alone or together with adenosine diphosphate (ADP) or thrombin PAR1 receptor-activating peptide (TRAP). We found that in the absence of other activators, protamine (80 mu g/mL) increased the proportion of platelets with active fibrinogen receptor (binding of PAC-1) from 3.6% to 97.0% (p < .001) measured with flow cytometry. Impedance aggregometry also increased slightly after exposure to protamine alone. When activated with ADP or TRAP protamine at 80 mu g/mL reduced aggregation, from 73.8 +/- 29.4 U to 46.9 +/- 21.1 U (p < .001) with ADP and from 126.4 +/- 16.1 U to 94.9 +/- 23.7 U (p < .01) with TRAP. P-selectin exposure (a marker of alpha-granule release) measured by median fluorescence intensity (MFI) increased dose dependently with protamine alone, from 0.76 +/- 0.20 (0 mu g/mL) to 10.2 +/- 3.1 (80 mu g/mL), p < .001. Protamine 80 mu g/mL by itself resulted in higher MFI (10.16 +/- 3.09) than activation with ADP (2.2 +/- 0.7, p < .001) or TRAP (5.7 +/- 2.6, p < .01) without protamine. When protamine was combined with ADP or TRAP, there was a concentration-dependent increase in the alpha-granule release. In conclusion, protamine interacts with platelets in vitro having both a direct activating effect and impairment of secondary activation of aggregation by other agonists.
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