20 most-cited countries in clinical medicine ranked by population size.
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Biomedical subjects
Publications and source records attributed to John Bailey.
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A large body of literature addresses the role of science in environmental impact assessment (EIA) but less attention has been given to the views of practitioners themselves. In this research a survey of 31 EIA practitioners in Western Australia was undertaken to determine their perceptions of the quality and importance of science in EIA. The survey results are compared with previous theoretical, empirical, and survey studies of the role of science in EIA. Interview questions addressed the role of science in impact prediction, monitoring activities, mitigation and management, and EIA decision-making. It was clear from the interviews that many practitioners are satisfied with the quality of science currently used in EIA, but do not believe that it is given sufficient importance in the process. The quality and importance of science in the predecision stages of EIA was rated higher than in the postdecision stages. While science was perceived to provide the basis for baseline data collection, impact prediction, and mitigation design, it was seen to be less important during decision-making and ongoing project management. Science was seen to be just one input to decision-makers along with other factors such as sociopolitical and economic considerations. While time and budget constraints were seen to limit the scientific integrity of EIA activities, pressure from the public and regulatory authorities increased it. Improving the scientific component of EIA will require consideration of all these factors, not just the technical issues.
We characterized the anti-viral T-cell response in 22 chronically infected patients, who participated in a European multi-center randomized placebo-controlled, double-blind study therapeutic vaccination trial with pre-S1, pre-S2 and S antigenic components of the hepatitis B virus (HBV). It induced a significant HBsAg-specific T-cell proliferation and the production of Th2-cytokines (i.e. IL-5). A specific induction of Th1-lymphokines was not detectable although this has been demonstrated in this study in response to the nucleocapsid protein (HBcAg). Further analysis indicated that this approach does not activate HBV-specific CD8+ T-lymphocytes as detected by ELISPOT-assay. Our results might explain why a specific therapeutic vaccine, although safe and well-tolerated is not always able to break tolerance leading to the clearance of the hepatitis B virus.
BACKGROUND: Vascular endothelial growth factor (VEGF) is a potent angiogenic cytokine, and various inhibitory agents, including specific antibodies, have been developed to block VEGF-stimulated angiogenesis. We developed HuMV833, a humanized version of a mouse monoclonal anti-VEGF antibody (MV833) that has antitumor activity against a number of human tumor xenografts, and investigated the distribution and biologic effects of HuMV833 in patients in a phase I trial. METHODS: Twenty patients with progressive solid tumors were treated with various doses of HuMV833 (0.3, 1, 3, or 10 mg/kg). Positron emission tomography with (124)I-HuMV833 was used to measure the antibody distribution in and clearance from tissues. Magnetic resonance imaging was used to measure the vascular permeability surface area product with a first-pass pharmacokinetic model (k(fp)) to determine tumor vascular permeability. RESULTS: The antibody was generally well tolerated, although the incremental dose, phase I study design, and pharmacodynamic endpoints could not identify the optimum biologically active dose. Antibody distribution and clearance were markedly heterogeneous between and within patients and between and within individual tumors. HuMV833 distribution to normal tissues also varied among patients, but the antibody was cleared from these tissues in a homogeneous fashion. Permeability was strongly heterogeneous between and within patients and between and within individual tumors. All tumors showed a reduction in k(fp) 48 hours after the first treatment (median = 44%; range = 4%-91%). CONCLUSIONS: Because of the heterogeneity in tumor biology with respect to antibody uptake and clearance, we suggest that either intrapatient dose escalation approaches or larger, more precisely defined patient cohorts would be preferable to conventional strategies in the design of phase I studies with antiangiogenic compounds like HuMV833.
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OBJECTIVES: To estimate the contribution of driver sleepiness to the causes of car crash injuries. DESIGN: Population based case control study. SETTING: Auckland region of New Zealand, April 1998 to July 1999. PARTICIPANTS: 571 car drivers involved in crashes where at least one occupant was admitted to hospital or killed ("injury crash"); 588 car drivers recruited while driving on public roads (controls), representative of all time spent driving in the study region during the study period. MAIN OUTCOME MEASURES: Relative risk for injury crash associated with driver characteristics related to sleep, and the population attributable risk for driver sleepiness. RESULTS: There was a strong association between measures of acute sleepiness and the risk of an injury crash. After adjustment for major confounders significantly increased risk was associated with drivers who identified themselves as sleepy (Stanford sleepiness score 4-7 v 1-3; odds ratio 8.2, 95% confidence interval 3.4 to 19.7); with drivers who reported five hours or less of sleep in the previous 24 hours compared with more than five hours (2.7, 1.4 to 5.4); and with driving between 2 am and 5 am compared with other times of day (5.6, 1.4 to 22.7). No increase in risk was associated with measures of chronic sleepiness. The population attributable risk for driving with one or more of the acute sleepiness risk factors was 19% (15% to 25%). CONCLUSIONS: Acute sleepiness in car drivers significantly increases the risk of a crash in which a car occupant is injured or killed. Reductions in road traffic injuries may be achieved if fewer people drive when they are sleepy or have been deprived of sleep or drive between 2 am and 5 am.