Microfacies, Depositional Environments, and Diagenesis of the Amapa Carbonates (paleocene-Middle Miocene), Foz Do Amazonas Basin, Offshore Ne Brazil

195 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1984.A total of 2,795 thin sections were studied, representing the carbonate section of 18 wells drilled in the Foz do Amazonas Basin, offshore northeast Brazil. The Amapa Formation (Paleocene-Middle Miocene) consists of a carbonate platform adjacent to a landward fluvio-deltaic system which periodically prograded over the platform. The latter became discontinuous in the central portion of the basin after the Oligocene, when transverse canyons were developed connecting the deltaic complex to the open sea.The Amapa carbonates have been divided into 22 distinct microfacies combined into two depositional models separated by a major unconformity. The paleoenvironmental reconstruction of model 1 (Paleocene to Early Eocene) consists of five juxtaposed microfacies classified into three environmental subdivisions. Model 2 (Middle Eocene to Middle Miocene) comprises 17 microfacies classified into seven subenvironments.A sequence of twelve diagenetic stages was established for model 1 based on textural relationships. The most important reservoir rocks in this model are due to primary porosity locally reduced by later cementation. These potential oil reservoirs, which locally reach 20% porosity consist of lagoonal deposits of dasycladacean calcarenites with common intraparticle and interparticle porosity. The diagenetic sequence determined for model 2 comprises 13 distinct events. The best reservoirs in this model are due to secondary porosity generated by both selective and nonselective dissolution, the underground freshwater circulation being the main control factor of porosity generation.In the basinwide diagenetic interpretation it is suggested that four episodes of sea level lowering disrupted the dynamic equilibrium existing between rivers and ocean, and triggered distinct reactivations of the groundwater system. These disruptions would have activated extensive underground circulations of freshwater through the carbonates, causing both porosity generation in the undersaturated zone and dolomitization in the mixed water zone.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

Edoxaban versus warfarin in patients with atrial fibrillation

Contains fulltext : 125374.pdf (publisher's version ) (Open Access)BACKGROUND: Edoxaban is a direct oral factor Xa inhibitor with proven antithrombotic effects. The long-term efficacy and safety of edoxaban as compared with warfarin in patients with atrial fibrillation is not known. METHODS: We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding. RESULTS: The annualized rate of the primary end point during treatment was 1.50% with warfarin (median time in the therapeutic range, 68.4%), as compared with 1.18% with high-dose edoxaban (hazard ratio, 0.79; 97.5% confidence interval [CI], 0.63 to 0.99; P<0.001 for noninferiority) and 1.61% with low-dose edoxaban (hazard ratio, 1.07; 97.5% CI, 0.87 to 1.31; P=0.005 for noninferiority). In the intention-to-treat analysis, there was a trend favoring high-dose edoxaban versus warfarin (hazard ratio, 0.87; 97.5% CI, 0.73 to 1.04; P=0.08) and an unfavorable trend with low-dose edoxaban versus warfarin (hazard ratio, 1.13; 97.5% CI, 0.96 to 1.34; P=0.10). The annualized rate of major bleeding was 3.43% with warfarin versus 2.75% with high-dose edoxaban (hazard ratio, 0.80; 95% CI, 0.71 to 0.91; P<0.001) and 1.61% with low-dose edoxaban (hazard ratio, 0.47; 95% CI, 0.41 to 0.55; P<0.001). The corresponding annualized rates of death from cardiovascular causes were 3.17% versus 2.74% (hazard ratio, 0.86; 95% CI, 0.77 to 0.97; P=0.01), and 2.71% (hazard ratio, 0.85; 95% CI, 0.76 to 0.96; P=0.008), and the corresponding rates of the key secondary end point (a composite of stroke, systemic embolism, or death from cardiovascular causes) were 4.43% versus 3.85% (hazard ratio, 0.87; 95% CI, 0.78 to 0.96; P=0.005), and 4.23% (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.32). CONCLUSIONS: Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes. (Funded by Daiichi Sankyo Pharma Development; ENGAGE AF-TIMI 48 ClinicalTrials.gov number, NCT00781391.)