In the current study, delirium occurred in 44% of elderly patients after a major operation. Pre-existing cognitive dysfunction was the strongest predictor of the development of postoperative delirium. Outcomes, including an increased rate of 6 month mortality, were worse in patients who developed postoperative delirium.
BackgroundAcute renal failure from ischemia significantly contributes to morbidity and mortality in clinical settings, and strategies to improve renal resistance to ischemia are urgently needed. Here, we identified a novel pathway of renal protection from ischemia using ischemic preconditioning (IP).Methods and FindingsFor this purpose, we utilized a recently developed model of renal ischemia and IP via a hanging weight system that allows repeated and atraumatic occlusion of the renal artery in mice, followed by measurements of specific parameters or renal functions. Studies in gene-targeted mice for each individual adenosine receptor (AR) confirmed renal protection by IP in A1−/−, A2A−/−, or A3AR−/− mice. In contrast, protection from ischemia was abolished in A2BAR−/− mice. This protection was associated with corresponding changes in tissue inflammation and nitric oxide production. In accordance, the A2BAR-antagonist PSB1115 blocked renal protection by IP, while treatment with the selective A2BAR-agonist BAY 60–6583 dramatically improved renal function and histology following ischemia alone. Using an A2BAR-reporter model, we found exclusive expression of A2BARs within the reno-vasculature. Studies using A2BAR bone-marrow chimera conferred kidney protection selectively to renal A2BARs.ConclusionsThese results identify the A2BAR as a novel therapeutic target for providing potent protection from renal ischemia.
Our purpose was to determine the relationship between habitual aerobic exercise status and the rate of decline in maximal aerobic capacity across the adult age range in women. A meta-analytic approach was used in which mean maximal oxygen consumption (VO2 max) values from female subject groups (ages 18-89 yr) were obtained from the published literature. A total of 239 subject groups from 109 studies involving 4,884 subjects met the inclusion criteria and were arbitrarily separated into sedentary (groups = 107; subjects = 2,256), active (groups = 69; subjects = 1, 717), and endurance-trained (groups = 63; subjects = 911) populations. VO2 max averaged 29.7 +/- 7.8, 38.7 +/- 9.2, and 52.0 +/- 10.5 ml . kg-1 . min-1, respectively, and was inversely related to age within each population (r = -0.82 to -0.87, all P < 0.0001). The rate of decline in VO2 max with increasing subject group age was lowest in sedentary women (-3.5 ml . kg-1 . min-1 . decade-1), greater in active women (-4.4 ml . kg-1 . min-1 . decade-1), and greatest in endurance-trained women (-6.2 ml . kg-1 . min-1 . decade-1) (all P < 0.001 vs. each other). When expressed as percent decrease from mean levels at age approximately 25 yr, the rates of decline in VO2 max were similar in the three populations (-10.0 to -10.9%/decade). There was no obvious relationship between aerobic exercise status and the rate of decline in maximal heart rate with age. The results of this cross-sectional study support the hypothesis that, in contrast to the prevailing view, the rate of decline in maximal aerobic capacity with age is greater, not smaller, in endurance-trained vs. sedentary women. The greater rate of decline in VO2 max in endurance-trained populations may be related to their higher values as young adults (baseline effect) and/or to greater age-related reductions in exercise volume; however, it does not appear to be related to a greater rate of decline in maximal heart rate with age.
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