John I. Kennedy
University of Alabama at Birmingham
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Featured researches published by John I. Kennedy.
The American Journal of Medicine | 2016
Andrew E. Epstein; Brian Olshansky; Gerald V. Naccarelli; John I. Kennedy; Elizabeth Murphy; Nora Goldschlager
Amiodarone, an iodinated benzofuran derivative with Class I, II, III, and IV antiarrhythmic properties, is the most commonly used antiarrhythmic drug used to treat supraventricular and ventricular arrhythmias. Appropriate use of this drug, with its severe and potentially life-threatening adverse effects, requires an essential understanding of its risk-benefit properties in order to ensure safety. The objective of this review is to afford clinicians who treat patients receiving amiodarone an appropriate management strategy for its safe use. The authors of this consensus management guide have thoroughly reviewed and evaluated the existing literature on amiodarone and apply this information, along with the collective experience of the authors, in its development. Provided are management guides on the intravenous and oral dosing of amiodarone, appropriate outpatient follow-up of patients taking the drug, its recognized adverse effects, and recommendations on when to consult specialists to help in patient management. All clinicians must be cognizant of the appropriate use, follow-up, and adverse reactions of amiodarone. The responsibility incurred by those treating such patients cannot be overemphasized.
The American Journal of Medicine | 2009
Gregory C. Kane; Michael R. Grever; John I. Kennedy; Mary Ann Kuzma; Alan R. Saltzman; Peter H. Wiernik; Nicole V. Baptista
he Anticipated Physician Shortage: Meeting the ation’s Need for Physician Services regory C. Kane, MD, Michael R. Grever, MD, John I. Kennedy, MD, Mary Ann Kuzma, MD, lan R. Saltzman, MD, Peter H. Wiernik, MD, Nicole V. Baptista, BS Division of Pulmonary Medicine and Critical Care, Department of Medicine, Jefferson Medical College, Philadelphia, Pa; Department of Internal Medicine, Ohio State University College of Medicine, Columbus; Department of Medicine, niversity of Alabama at Birmingham School of Medicine, Birmingham; Birmingham VA Medical Center; Department of edicine, Drexel University College of Medicine, Philadelphia, Pa; Department of Medicine, State University of New York t Buffalo School of Medicine and Biomedical Sciences, Buffalo; Division of Hematology and Oncology, Department of nternal Medicine, New York Medical College (Our Lady of Mercy), Bronx, NY; Alliance for Academic Internal Medicine, ashington, DC.
Experimental Lung Research | 1989
John I. Kennedy; David B. Chandler; Jack D. Fulmer; Michael B. Wert; William E. Grizzle
Intratracheal bleomycin induces pulmonary fibrosis in experimental animals, but the mechanisms involved are poorly understood. Since altered levels of fatty acid metabolites are associated with bleomycin-induced lung injury, we examined the effects of a change in dietary fat on bleomycin-induced fibrosis. Previously we have shown that an essential fatty acid-deficient diet can reduce the severity of bleomycin-induced pulmonary fibrosis. The present study examined the effect of replacement of usual dietary fat with menhaden oil, rich in eicosapentaenoic acid, on the development of pulmonary fibrosis. Weanling rats were raised on a standard laboratory diet or a diet consisting of a fat-free powder to which was added 25% (w/w) of menhaden oil. After 8 weeks of feeding, the animals received either 1.5 units of bleomycin or an equivalent volume of saline intratracheally. In animals receiving the laboratory diet, bleomycin treatment produced a 44% increase in total lung protein content when compared to saline-treated controls (p less than 0.001) and a 77% increase in total lung hydroxyproline content (p less than 0.01). In contrast, bleomycin-treated animals receiving the menhaden oil diet had only small increases, which did not reach statistical significance, in protein and hydroxyproline content in the lung. Bronchoalveolar lavage cellularity did not differ among the treatment groups, but the percentage of lavage macrophages was slightly diminished in bleomycin-treated animals receiving the laboratory diet. Cellular differentials of lavage fluid did not differ significantly between bleomycin- and saline-treated animals receiving the menhaden oil diet. Bleomycin-induced histologic changes, quantitated by morphometric analysis, were significantly reduced with the menhaden oil diet. We conclude that a diet rich in eicosapentaenoic acid can significantly ameliorate bleomycin-induced pulmonary fibrosis, possibly via alterations in eicosanoid metabolism.
Experimental Lung Research | 1987
John I. Kennedy; David B. Chandler; Jack D. Fulmer; Michael B. Wert; William E. Grizzle
Bleomycin treatment has been used for the experimental induction of pulmonary fibrosis, but the mechanisms involved are poorly understood. Since alterations in the levels of certain fatty acid metabolites have been associated with bleomycin-induced lung injury, we examined the effects of different dietary fats on the development of bleomycin-induced pulmonary fibrosis. Weanling rats were raised on standard laboratory feed or a diet consisting of a fat-free powder to which was added either coconut oil or beef tallow (25% w/w). After 8 weeks of feeding, animals received either 1.5 units bleomycin or an equivalent volume of saline intratracheally. Bleomycin treatment resulted in significant increases in total lung hydroxyproline content in the groups fed the standard lab diet (p less than 0.001) and beef tallow diet (p less than 0.001), but not in the group receiving the coconut oil diet. Furthermore, the lung hydroxyproline content in bleomycin-treated animals was less with the beef tallow diet compared with standard lab feed (p less than 0.05). Bleomycin treatment resulted in an increase in thiobarbituric acid-reactive products, an index of lipid peroxidation, in lungs from animals fed the standard lab diet, but not in the other diet groups. The percentage of diseased lung, as determined by morphometric analysis, was increased in bleomycin-treated animals from all diet groups (p less than 0.05). We conclude that alterations in dietary fats can reduce the severity of pulmonary fibrosis resulting from bleomycin treatment. Possible mechanisms for this effect include alterations in eicosanoid metabolism or changes in immune or effector cell function.
JAMA Internal Medicine | 1987
John I. Kennedy; Jeffrey L. Myers; Vance J. Plumb; Jack D. Fulmer
Chest | 1992
Robert Bruce Gammon; Tracy A. Bridges; Hussein Al-Nezir; Charles Bruce Alexander; John I. Kennedy
The American review of respiratory disease | 1988
David B. Chandler; James C. Barton; D.D. Briggs; Thomas W. Butler; John I. Kennedy; William E. Grizzle; Jack D. Fulmer
The American review of respiratory disease | 2015
David B. Chandler; John I. Kennedy; Jack D. Fulmer
Chest | 1986
John I. Kennedy; David B. Chandler; Robert M. Jackson; Jack D. Fulmer
Chest | 1985
John I. Kennedy; Jack D. Fulmer