Eight asthmatic patients and two normal subjects performed two identical exercise tests 140 minutes apart (first test preceded by inhalation of saline and the second by terbutaline sulphate). A ninth asthmatic patient exercised twice after placebo 40 minutes apart. Arterial plasma levels of histamine and cyclic AMP, expiratory flow rates and volumes were measured at rest and during and after exercise. After the first test the mean+SEM fall in PEFR was 45 2±2-6%. In five asthmatics there was an increase in plasma histamine (mean±SEM 14-8±3-3 pmol ml-') coinciding with exercise-induced asthma (EIA). Histamine levels returned to pre-exercise values within 30 minutes. After terbutaline these five patients had histamine levels greater than those observed before, during, or after the first test. This effect may have been the result of changes in pulmonary microcirculation. After the second test the levels decreased indicating no further release of histamine in response to exercise. No EIA occurred in these patients after terbutaline. The other patients and the two normal subjects had little or no change in histamine throughout the study. The one patient in whom exercise was repeated after placebo demonstrated less histamine release and less EIA after the second test.As early as 1966 McNeill and his associates' suggested that chemical mediators of bronchoconstriction such as histamine and slow reacting substance of anaphylaxis (SRS-A) may be released in response to exercise. The evidence for mediator release as a causal factor in exercise-induced asthma (EIA) has been derived from studies of repeated exercise challenge and the prevention of EIA by pharmacological inhibitors of varying specificity. The occurrence of a refractory period in some patients when exercise challenge is repeated within one hour2 3 is consistent with the hypothesis that mediators are depleted as a result of the initial exercise and take some time to be replenished. Furthermore, drugs which inhibit antigen-induced mediator release in vitro such as diethylcarbamazine,4 sodium cromoglycate,5 and the betaadrenoceptor agonists6 prevent EIA in a significant proportion of asthmatic patients.7 8
The implementation of CoC standard 3.3 represents a paradigm shift in the care of cancer survivors, with a statement that treatment summaries and survivorship care plans are important documents for patient care and should be required.
Cancer leaders assess the impact on the cancer patient of the historic passage of Patient Protection and Affordable Care Act (HR 3590) (PPACA). The Association of Cancer Executives, a national organization for leadership development of oncology executives and improvements in patient care delivery, and the Association of Community Cancer Centers, a leading education and advocacy organization for the cancer team, weigh in on the impact of PPACA. Oncology leaders assess the impact of PPACA on cancer patients and families, cancer programs in the United States, and provider relations. The provisions of PPACA most impacting cancer patients are reviewed, including reimbursement changes, expansion of prevention and screening services, the development of accountable care organizations, physician relations, and the implementation of integrated electronic health records. Cancer executives prepare their programs for PPACA by changing the care delivery model to ensure the economic survival of private practices and hospital-based programs.
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