Faculty Bibliography

UNITED NATIONS - Prompted by fears of a new outbreak of one of the world's deadliest scourges, the World Health Assembly in Geneva effectively decided Friday to defer eradicating the world's known remaining stocks of the smallpox virus until at least 2002. While virtually all member states said they remained committed to the elimination of the smallpox stocks as soon as possible, the action taken by a key committee acting on consensus, without a formal vote, reflected widespread agreement that more time is needed to study smallpox before it's irrevocably destroyed. Both Washington and Moscow have publicly opposed eradication of the virus, at least until more research is done. Though smallpox was officially declared eradicated as a disease in 1980, most officials now acknowledge there probably are clandestine smallpox stocks throughout the world, and that retaining the virus could speed the development of new drugs to fight an outbreak that occurred either naturally or as a result of bioterrorism. A turning point in official U.S. thinking about the virus's fate came in March, when an independent scientific panel concluded research on the deadly smallpox virus could provide important scientific and medical opportunities that would be lost if the virus were destroyed

Prompted by fears of a new outbreak of one of the world\'s deadliest scourges, the World Health Assembly in Geneva effectively decided yesterday to defer eradicating the world\'s known remaining stocks of the smallpox virus until at least 2002. While virtually all member states said they remained committed to the elimination of the smallpox stocks as soon as possible, the action taken by a key committee acting on consensus, without a formal vote, reflected widespread agreement that more time is needed to study smallpox before it is irrevocably destroyed. The decision reflects a major shift in scientific thinking about the virus since 1996, when the Assembly decided it should be destroyed at the end of June 1999. It highlighted the existence of increasingly rare political common ground between the United States and Russia, the two remaining repositories of the deadly stocks. Both Washington and Moscow have publicly opposed eradication of the virus, at least until more research is done

Prompted by fears of a new outbreak of one of the world's deadliest scourges, the World Health Assembly in Geneva effectively decided Friday to defer eradicating the world's known remaining stocks of the smallpox virus until at least 2002. While virtually all member states said they remained committed to the elimination of the smallpox stocks as soon as possible, the move by a key committee acting on consensus, without a formal vote, reflected widespread agreement that more time is needed to study smallpox before it is irrevocably destroyed. Friday's recommendation came from a panel of the World Health Assembly, the highest governing body of the World Health Organization. The committee's recommendations are to be formally approved early next week

Prompted by fears of a new outbreak of one of the world's deadliest scourges, the World Health Assembly in Geneva effectively decided Friday to defer eradicating the world's known remaining stocks of the smallpox virus until at least 2002. While virtually all member states said they remained committed to the elimination of the smallpox stocks as soon as possible, the action taken by a key committee acting on consensus, without a formal vote, reflected widespread agreement that more time is needed to study smallpox before it is irrevocably destroyed

Prompted by fears of a new outbreak of one of the world's deadliest scourges, the World Health Assembly in Geneva effectively decided yesterday to defer eradicating the world's known remaining stocks of the smallpox virus until at least 2002

BACKGROUND: Low-molecular-weight heparins may simplify the management of deep venous thrombosis. A critical clinical issue is whether this more convenient therapy is as safe and effective as treatment with unfractionated heparin. PURPOSE: To compare the safety and efficacy of low-molecular-weight heparins with those of unfractionated heparin for treatment of acute deep venous thrombosis. DATA SOURCES: Reviewers identified studies by searching MEDLINE, reviewing references from retrieved articles, scanning abstracts from conference proceedings, and contacting investigators and pharmaceutical companies. STUDY SELECTION: Randomized, controlled trials that compared a low-molecular-weight heparin preparation with unfractionated heparin for treatment of acute deep venous thrombosis. DATA EXTRACTION: Two reviewers extracted data independently. Reviewers evaluated study quality using a validated four-item instrument. DATA SYNTHESIS: Eleven of 37 studies met inclusion criteria for three major outcomes. Most studies used proper randomization procedures, but only one was double-blinded. Compared with unfractionated heparin, low-molecular-weight heparins reduced mortality rates over 3 to 6 months of patient follow-up (odds ratio, 0.71 [95% CI, 0.53 to 0.94]; P = 0.02). For major bleeding complications, the odds ratio favored low-molecular-weight heparins (0.57 [CI, 0.33 to 0.99]; P = 0.047), but the absolute risk reduction was small and not statistically significant (0.61% [CI, -0.04% to 1.26%]; P = 0.07). For preventing thromboembolic recurrences, low-molecular-weight heparins seemed as effective as unfractionated heparin (odds ratio, 0.85 [CI, 0.63 to 1.14]; P > 0.2). CONCLUSIONS: Low-molecular-weight heparin treatment reduces mortality rates after acute deep venous thrombosis. These drugs seem to be as safe as unfractionated heparin with respect to major bleeding complications and appear to be as effective in preventing thromboembolic recurrences

BACKGROUND: Low-molecular-weight heparins are effective for treating venous thrombosis, but their cost-effectiveness has not been rigorously assessed. OBJECTIVE: To evaluate the cost-effectiveness of low-molecular-weight heparins compared with unfractionated heparin for treatment of acute deep venous thrombosis. DESIGN: Decision model. DATA SOURCES: Probabilities for clinical outcomes were obtained from a meta-analysis of randomized trials. Cost estimates were derived from Medicare reimbursement and other sources. TARGET POPULATION: Two hypothetical cohorts of 60-year-old men with acute deep venous thrombosis. TIME HORIZON: Patient lifetime. PERSPECTIVE: Societal. INTERVENTION: Fixed-dose low-molecular-weight heparin or adjusted-dose unfractionated heparin. OUTCOME MEASURES: Costs, quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios. An in-patient hospital setting was used for the base-case analysis. Secondary analyses examined outpatient treatment with low-molecular-weight heparin. RESULTS OF BASE-CASE ANALYSIS: Total costs for inpatient treatment were $26,516 for low-molecular-weight heparin and $26,361 for unfractionated heparin. The cost of initial care was higher in patients who received low-molecular-weight heparin, but this was partly offset by reduced costs for early complications. Low-molecular-weight heparin treatment increased quality-adjusted life expectancy by approximately 0.02 years. The incremental cost-effectiveness of inpatient low-molecular-weight heparin treatment was $7820 per QALY gained. Treatment with low-molecular-weight heparin was cost saving when as few as 8% of patients were treated at home. RESULTS OF SENSITIVITY ANALYSIS: When late complications were assumed to occur 25% less frequently in patients who received unfractionated heparin, the incremental cost-effectiveness ratio increased to almost $75,000 per QALY gained. When late complications were assumed to occur 25% less frequently in patients who received low-molecular-weight heparin, this treatment resulted in a net cost savings. Inpatient low-molecular-weight heparin treatment became cost saving when its pharmacy cost was reduced by 31% or more, when it reduced the yearly incidence of late complications by at least 7%, when as few as 8% of patients were treated entirely as outpatients, or when at least 13% of patients were eligible for early discharge. CONCLUSIONS: Low-molecular-weight heparins are highly cost-effective for inpatient management of venous thrombosis. This treatment reduces costs when small numbers of patients are eligible for outpatient management

Little known fact: About 1 million Americans suffer from gout - yes, gout, that old-fashioned-sounding illness with symptoms that are sudden,..

In the freshwater coelenterate, hydra, asexual reproduction via budding occurs at the base of the gastric region about two-thirds of the distance from the head to the foot. Developmental gradients of head and foot activation and inhibition originating from these organizing centers have long been assumed to control budding in hydra. Much has been learned over the years about these developmental gradients and axial pattern formation, and in particular, the inhibitory influence of the head on budding is well documented. However, understanding of the role of the foot and potential interactions between the foot, bud, and head patterning systems is lacking. The purpose of this study was to investigate the role of the foot in the initiation of new axis formation during budding by manipulating the foot and monitoring effects on the onset of first bud evagination and the time necessary to reach the 50% budding point. Several experimental situations were examined: the lower peduncle and foot (PF) were injured or removed, a second PF was laterally grafted onto animals either basally (below the budding zone) or apically (above the budding zone), or both the head and PF were removed simultaneously. When the PF was injured or removed, the onset of first bud evagination was delayed and/or the time until the 50% budding point was reached was longer. The effects were more pronounced when the manipulation was performed closer to the anticipated onset of budding. When PF tissue was doubled, precocious bud evagination was induced, regardless of graft location. Removal of the PF at the same time as decapitation reduced the inductive effect of decapitation on bud evagination. These results are discussed in light of potential signals from the foot or interactions between the foot and head patterning systems that might influence bud axis initiation

Peering into a standard microscope at tissues from the boy's autopsy, Dr. Ralph Douglas Kenneth Reye found no evidence of infection. Instead, he noticed distinct liver and brain damage of a type that he had never seen. Over the next 11 years at the Royal Alexandra Hospital for Children, Dr. Reye identified 20 more cases of what his colleagues nicknamed Reye's syndrome. The doctors suspected the damage had resulted from a toxin they could not identify. In 1963, Dr. Reye (pronounced like rye) described the cases in The Lancet. Although the report came from the same hospital where in 1942 Dr. Norman Gregg first recognized the damage that rubella virus infection in a pregnant woman could cause in her fetus, Reye's syndrome drew little attention. Still, these reports started a chain of events that led to one of the century's major public health triumphs, while leaving the man the syndrome was named for nearly obscure. Although Reye's syndrome bears one name, it took many scientists elsewhere to make it a public health success story. It also took two colleagues, Dr. Graeme Morgan and Dr. Jim Baral, to push Dr. Reye to publish his findings about the syndrome. Dr. Baral said that when he began training at the hospital in 1961, one of his first patients was admitted with the diagnosis of Reye's syndrome. Dr. Baral had never heard of it. So he consulted textbooks and journals