Frisch and colleagues (1985) reported that women who did not participate in collegiate athletics were at 1.86 times greater risk of breast cancer relative to collegiate athletes, 82% of whom were physically active in adolescence and 74% of whom maintained high physical activity levels into adulthood. Most subsequent studies have provided evidence for a reduced risk of breast cancer among women with high levels of physical activity (Friedenreich et al, 1998b). Inconsistencies in previous studies may be partly due to inadequate measures of long-term physical activity. Two recent prospective studies employing multiple measures of physical activity in adulthood have reported 20 to 50% reductions in risk (Thune et al, 1997;Rockhill et al, 1999). While case-control studies may be more susceptible to recall and selection biases, they offer the opportunity, unavailable in most prospective studies, to obtain more comprehensive assessments of lifetime physical activity.As few recent studies have done so, we have examined the effects of lifetime occupational physical activity, and the independent effects on breast cancer risk of exercise in adolescence and adulthood, both separately and together as well as changes between adolescence and adulthood.
MATERIALS AND METHODSStudy design and participant recruitment. Relevant bodies approved the methodology for the Shanghai Breast Cancer Study and a detailed description of the study has been published elsewhere (Gao et al, 2000). Briefly, this was a population-based case-control study designed to recruit all incident breast cancer cases aged 25 to 64 years among permanent residents of urban Shanghai between August 1996 and March 1998. All study participants had no prior history of cancer and were alive at the time of interview. Through a rapid case-ascertainment system, supplemented by the population-based Shanghai Cancer Registry, 1602 eligible breast cancer cases were identified during the study period, and in-person interviews were completed for 1459 (91.1%) of them. The major reasons for non-participation were refusal (109 cases, 6.8%), death prior to interview (17 cases, 1.1%), and inability to locate (17 cases, 1.1%). Two senior pathologists confirmed the diagnoses.Controls were randomly selected from permanent female residents of urban Shanghai and frequency-matched to cases by age. The number of controls in each age-specific stratum was determined in advance using the age distribution of the incident breast cancer cases reported to the Shanghai Cancer Registry from 1990 to 1993. This registry, which keeps cards for all permanent residents of urban Shanghai, was used to select controls. For each age-predetermined control, a registry card for a potential control in the same 5-year age group was randomly selected. In-person interviews were completed for 1556 (90.3%) of the 1724 eligible controls identified. Only 166 (9.6%) controls refused participation and 2 (0.1%) controls were excluded because they were deceased.
MeasurementsTrained interviewers used a structured questio...
We determined the roles of liver and splanchnic vascular bed in anaphylactic hypotension in anesthetized rats and the effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused rat livers. In anesthetized rats sensitized with ovalbumin (1 mg), an intravenous injection of 0.6 mg ovalbumin caused not only a decrease in systemic arterial pressure from 120 +/- 9 to 43 +/- 10 mmHg but also an increase in portal venous pressure that persisted for 20 min after the antigen injection (the portal hypertension phase). The elimination of the splanchnic vascular beds, by the occlusions of the celiac and mesenteric arteries, combined with total hepatectomy attenuated anaphylactic hypotension during the portal hypertension phase. For the isolated perfused rat liver experiment, the livers derived from sensitized rats were hemoperfused via the portal vein at a constant flow. Using the double-occlusion technique to estimate the hepatic sinusoidal pressure, presinusoidal (R(pre)) and postsinusoidal (R(post)) resistances were calculated. An injection of antigen (0.015 mg) caused venoconstriction characterized by an almost selective increase in R(pre) rather than R(post) and liver weight loss. Taken together, these results suggest that liver and splanchnic vascular beds are involved in anaphylactic hypotension presumably because of anaphylactic presinusoidal contraction-induced portal hypertension, which induced splanchnic congestion resulting in a decrease in circulating blood volume and thus systemic arterial hypotension.
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