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Sökning: WFRF:(Walker K.A.)

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1.
  • Weinstein, J. N., et al. (författare)
  • The cancer genome atlas pan-cancer analysis project
  • 2013
  • Ingår i: Nature Genetics. - 1061-4036. ; 45:10, s. 1113-1120
  • Tidskriftsartikel (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.
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  • Atanasova, L., et al. (författare)
  • g-factor Measurements at RISING: The Cases of 127Sn and 128Sn
  • 2010
  • Ingår i: Europhysics Letters. - IOP Publishing. - 1286-4854 .- 0295-5075. ; 91:4, s. 42001
  • Tidskriftsartikel (refereegranskat)abstract
    • We report on g-factor measurements of the 19/2(+) T-1/2 = 4.5(3) mu s isomer in Sn-127 and the 10(+) T-1/2 = 2.69(23) mu s isomer in Sn-128. These isomers were produced and spin-aligned in relativistic heavy-ion fragmentation at GSI and were selected and separated by the GSI fragment separator ( FRS). The gamma-rays of the isomeric decay were detected by the RISING gamma-ray spectrometer. The method of time-differential perturbed angular distributions was utilized. The measured g-factors, g(19/2(+); Sn-127) =-0.17(2) and g(10(+); Sn-128)=-0.20(4), are compared with shell model calculations. The measured g-factors confirm the predominantly nu h(11/2)(-2) and nu(s(1/2)(-1) h(11/2)(-2)) character of the 10(+) and 19/2(-) isomers in Sn-128 and Sn-127, respectively. The results demonstrate the feasibility of the method for similar measurements in exotic neutron-rich nuclei. Copyright (C) EPLA, 2010
4.
  • Carleer, M. R., et al. (författare)
  • Validation of water vapour profiles from the Atmospheric Chemistry Experiment (ACE)
  • 2008
  • Ingår i: Atmospheric Chemistry and Physics Discussion: An Interactive Open Access Journal of the European Geosciences Union. ; 8:2, s. 4499-4559
  • Tidskriftsartikel (refereegranskat)abstract
    • The Atmospheric Chemistry Experiment (ACE) mission was launched in August 2003 to sound the atmosphere by solar occultation. Water vapour (H2O), one of the most important molecules for climate and atmospheric chemistry, is one of the key species provided by the two principal instruments, the infrared Fourier Transform Spectrometer (ACE-FTS) and the MAESTRO UV-Visible spectrometer (ACE-MAESTRO). The first instrument performs measurements on several lines in the 1362–2137 cm−1 range, from which vertically resolved H2O concentration profiles are retrieved, from 7 to 90 km altitude. ACE-MAESTRO measures profiles using the water absorption band in the near infrared part of the spectrum at 926.0–969.7 nm. This paper presents a comprehensive validation of the ACE-FTS profiles. We have compared the H2O volume mixing ratio profiles with space-borne (SAGE II, HALOE, POAM III, MIPAS, SMR) observations and measurements from balloon-borne frostpoint hygrometers and a ground based lidar. We show that the ACE-FTS measurements provide H2O profiles with small retrieval uncertainties in the stratosphere (better than 5% from 15 to 70 km, gradually increasing above). The situation is unclear in the upper troposphere, due mainly to the high variability of the water vapour volume mixing ratio in this region. A new water vapour data product from the ACE-MAESTRO (Measurement of Aerosol Extinction in the Stratosphere and Troposphere Retrieved by Occultation) is also presented and initial comparisons with ACE-FTS are discussed.
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6.
  • Danesh, John, et al. (författare)
  • Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis
  • 2005
  • Ingår i: JAMA : the journal of the American Medical Association. - American Medical Association. - 1538-3598. ; 294:14, s. 1799-1809
  • Forskningsöversikt (refereegranskat)abstract
    • CONTEXT: Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. DATA SOURCES: Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. STUDY SELECTION: All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. DATA EXTRACTION: Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. DATA SYNTHESIS: Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. CONCLUSIONS: In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.
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7.
  • Danesh, J., et al. (författare)
  • Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis
  • 2005
  • Ingår i: JAMA. - 1538-35980098-7484. ; 294:14, s. 1799-809
  • Tidskriftsartikel (refereegranskat)abstract
    • CONTEXT: Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. DATA SOURCES: Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. STUDY SELECTION: All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. DATA EXTRACTION: Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. DATA SYNTHESIS: Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. CONCLUSIONS: In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.
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