23 research outputs found

    Climate Change and Our Environment: The Effect on Respiratory and Allergic Disease

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    Climate change is a constant and ongoing process. It is postulated that human activities have reached a point at which we are producing global climate change. This article provides suggestions to help the allergist/environmental physician integrate recommendations about improvements in outdoor and indoor air quality and the likely response to predicted alterations in the earth’s environment into their patient’s treatment plan. Many changes that affect respiratory disease are anticipated. Examples of responses to climate change include energy reduction retrofits in homes that could potentially affect exposure to allergens and irritants, more hot sunny days that increase ozone-related difficulties, and rises in sea level or altered rainfall patterns that increase exposure to damp indoor environments. Climate changes can also affect ecosystems, manifested as the appearance of stinging and biting arthropods in new areas. Higher ambient carbon dioxide concentrations, warmer temperatures, and changes in floristic zones could potentially increase exposure to ragweed and other outdoor allergens, whereas green practices such as composting can increase allergen and irritant exposure. Finally, increased energy costs may result in urban crowding and human source pollution, leading to changes in patterns of infectious respiratory illnesses. Improved governmental controls on airborne pollutants could lead to cleaner air and reduced respiratory diseases but will meet strong opposition because of their effect on business productivity. The allergy community must therefore adapt, as physician and research scientists always have, by anticipating the needs of patients and by adopting practices and research methods to meet changing environmental conditions

    The Woody Guthrie Centennial Bibliography

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    This bibliography updates two extensive works designed to include comprehensively all significant works by and about Woody Guthrie. Richard A. Reuss published A Woody Guthrie Bibliography, 1912–1967 in 1968 and Jeffrey N. Gatten\u27s article “Woody Guthrie: A Bibliographic Update, 1968–1986” appeared in 1988. With this current article, researchers need only utilize these three bibliographies to identify all English-language items of relevance related to, or written by, Guthrie

    Prymnesins: Toxic Metabolites of the Golden Alga, Prymnesium parvum Carter (Haptophyta)

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    Increasingly over the past century, seasonal fish kills associated with toxic blooms of Prymnesium parvum have devastated aquaculture and native fish, shellfish, and mollusk populations worldwide. Protracted blooms of P. parvum can result in major disturbances to the local ecology and extensive monetary losses. Toxicity of this alga is attributed to a collection of compounds known as prymnesins, which exhibit potent cytotoxic, hemolytic, neurotoxic and ichthyotoxic effects. These secondary metabolites are especially damaging to gill-breathing organisms and they are believed to interact directly with plasma membranes, compromising integrity by permitting ion leakage. Several factors appear to function in the activation and potency of prymnesins including salinity, pH, ion availability, and growth phase. Prymnesins may function as defense compounds to prevent herbivory and some investigations suggest that they have allelopathic roles. Since the last extensive review was published, two prymnesins have been chemically characterized and ongoing investigations are aimed at the purification and analysis of numerous other toxic metabolites from this alga. More information is needed to unravel the mechanisms of prymnesin synthesis and the significance of these metabolites. Such work should greatly improve our limited understanding of the physiology and biochemistry of P. parvum and how to mitigate its blooms

    Successful Desensitization of a Patient with Aplastic Anemia to Antithymocyte Globulin

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    Antithymocyte globulin (ATG) is a polyclonal gamma immunoglobulin derived from either rabbit or equine serum that serves as therapy for aplastic anemia; however, ATG causes serum sickness in up to 70% and anaphylaxis in up to 5% of recipients. Intradermal (ID) skin testing has been the primary technique used to evaluate for a preexisting Gell and Coombs type I hypersensitivity reaction to ATG. There are no data reporting the predictive value of delayed reactions to ID testing on the risk of serum sickness. This study was designed to establish the importance of epicutaneous and ID skin testing before the administration of ATG through a case report and literature discussion. We report a patient with severe aplastic anemia that was successfully desensitized to ATG after a negative epicutaneous skin test and positive ID skin test. The patient had neither systemic nor localized reactions during the desensitization. Desensitization to ATG in patients with positive epicutaneous skin testing has been shown to be associated with serious and potentially life-threatening complications and should only be considered when the benefits outweigh the risks. Epicutaneous skin testing should be considered in conjunction with ID skin testing when screening for potential sensitivity to ATG. Because of the serious risk of anaphylaxis, desensitization should be performed in an intensive care unit setting in conjunction with a physician familiar with drug desensitization and the management of anaphylaxis
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