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2. Consensus standards for introductory e-learning courses in human participants research ethics

Author

Williams, John R, Sprumont, Dominique, Hirtle, Marie, Adebamowo, Clement, Braunschweiger, Paul, Bull, Susan, Burri, Christian, Czarkowski, Marek, Fan, Chien Te, Franck, Caroline, Gefenas, Eugenjius, Geissbuhler, Antoine, Klingmann, Ingrid, Kouyaté, Bocar, Kraehenbhul, Jean-Pierre, Kruger, Mariana, Moodley, Keymanthri, Ntoumi, Francine, Nyirenda, Thomas, Pym, Alexander, Silverman, Henry, and Tenorio, Sara

Published
2014

13. O PROGRAMA CITI: UMA ALTERNATIVA PARA A CAPACITAÇÃO NA ÉTICA DA PESQUISA NA AMÉRICA LATINA

Author

Litewka, Sergio, Goodman, Kenneth, and Braunschweiger, Paul

Subjects
Latin America, Portuguese, América Latina, human beings' protection, proteção dos sujeitos humanos, ética da pesquisa, investigation's ethics, Programa CITI, ética de la investigación, CITI Program, Spanish, protección de sujetos humanos
Abstract

El Programa CITI (Collaborative Institutional Training Initiative) es un curso basado en Internet y desarrollado por voluntarios, que brinda material educacional sobre protección de sujetos humanos en investigaciones biomédicas y de conducta, buenas prácticas clínicas, conducta responsable de la investigación y trato humanitario a animales de laboratorio. Es un esfuerzo conjunto del Fred Hutchinson Cancer Research Center y la Universidad de Miami. Con la colaboración de expertos locales, gran parte del contenido se ha adaptado para América Latina, se ha traducido al español y portugués y se han establecido acuerdos de colaboración con instituciones especializadas en bioética en Chile, Brasil, Costa Rica y Perú. Los autores presentan una metodología accesible para la capacitación en ética de la investigación y una justificación de su uso y difusión en América Latina. The CITI Program (Collaborative Institutional Training Initiative) is a course based on Internet with no profit intention; it has been developed by volunteers who offer educational subjects on human beings' protection in biomedical investigations, as well as on conduct, good medical practices, responsible conduct in investigation and humanitarian behaviour towards laboratory animals. This Program is a joint effort done by the Fred Hutchinson Cancer Research Centre and the University of Miami. With the collaboration of local experts a considerable part of its content has been adapted for Latin America, it has been translated to Spanish and Portuguese and collaborative agrees have been established with bioethics' specialized institutions in Chile, Brazil, Costa Rica and Peru. Its authors present an accessible methodology in order to train on investigation's ethics and to justify its use and spreading out throughout Latin America. O programa CITI (Iniciativa de treinamento institucional colaborativo) é um curso baseado na internet e desenvolvido por voluntários, que fornece material educacional sobre a proteção de sujeitos humanos nas pesquisas biomédicas e de conduta, boas práticas clínicas, conduta responsável da pesquisa e trato humanitário para animais em laboratório. É um esforço conjunto do Fred Hutchinson Câncer Research Center e a Universidade de Miami. Com a colaboração de peritos locais, grande parte do conteúdo foi adaptado para a América Latina e traduzido para o espanhol e português e se estabeleceram acordos de colaboração com instituições especializadas em bioética no Chile, Brasil,Costa Rica e, Peru. Os autores apresentam uma metodologia acessível para a capacitação em ética da pesquisa e uma justificação de seu uso e difusão na América Latina.

Published
2008

14. Consensus standards for introductory e-learning courses in human participants research ethics

Author

Williams, John R, primary, Sprumont, Dominique, additional, Hirtle, Marie, additional, Adebamowo, Clement, additional, Braunschweiger, Paul, additional, Bull, Susan, additional, Burri, Christian, additional, Czarkowski, Marek, additional, Fan, Chien Te, additional, Franck, Caroline, additional, Gefenas, Eugenjius, additional, Geissbuhler, Antoine, additional, Klingmann, Ingrid, additional, Kouyaté, Bocar, additional, Kraehenbhul, Jean-Pierre, additional, Kruger, Mariana, additional, Moodley, Keymanthri, additional, Ntoumi, Francine, additional, Nyirenda, Thomas, additional, Pym, Alexander, additional, Silverman, Henry, additional, and Tenorio, Sara, additional

Published
2013
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24. Dose Determination in High Dose-Rate Brachytherapy

Author

Houdek, Pavel V., primary, Schwade, James G., additional, Wu, Xiaodong, additional, Piscotta, Vincent, additional, Fiedler, Jeffrey A., additional, Serago, Christopher F., additional, Markoe, Arnold M., additional, Abitbol, Andre A., additional, Lewis, Alan A., additional, Braunschweiger, Paul G., additional, and Sklar, Marshall D., additional

Published
1993
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25. Accelerating hyperfractionation for carcinoma of the head and neck

Author

Schwade, James G., primary, Markoe, Arnold M., additional, Abitbol, Andre A., additional, Lewin, Alan A., additional, Brandon, Alfred H., additional, Houdek, Pavel, additional, Braunschweiger, Paul, additional, Casiano, Roy, additional, Sridhar, Kasi, additional, and Goodwin, W. Jarrard, additional

Published
1992
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26. Dose determination in high dose-rate brachytherapy

Author

Houdek, Pavel V., primary, Schwade, James G., additional, Wu, Xiaodong, additional, Pisciotta, Vincent, additional, Fiedler, Jeffrey A., additional, Serago, Christopher F., additional, Markoe, Arnold M., additional, Abitbol, Andre A., additional, Lewin, Alan A., additional, Braunschweiger, Paul G., additional, and Sklar, Marshall D., additional

Published
1992
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27. NEW NSF AND NIH RESPONSIBLE CONDUCT OF RESEARCH (RCR) GUIDELINES: A THREE-PHASE PLAN.

Author

McCafferty, Jennifer, Cushman, Reid, Goodman, Kenneth W., Braunschweiger, Paul, and Fiore, Robin N.

Subjects
RESEARCH ethics, UNITED States education system
Abstract

The article reports on the introduction of new guidelines on the Responsible Conduct of Research (RCR) from the U.S. National Institutes of Health (NIH) and the U.S National Science Foundation (NSF). It is said that the federal mandates for RCR education and training represent another unfunded mandate that must be implemented throughout the organization.

Published
2012

29. Acute Hemorrhagic Necrosis of Tumors Induced by Interleukin-1α Effects Independent of Tumor Necrosis Factor.

Author

Johnson, Candance S., Chang, Ming-jei, Braunschweiger, Paul G., and Furmanski, Philip

Abstract

Tumor necrosis factor (TNF), a protein synthesized in response to the endotoxin bacterial lipopolysaccharide (LPS), is the classical mediator of acute hemorrhagic necrosis of tumors. We have demonstrated that interleukin-la (IL-lα), with a spectrum of activities very similar to those of TNF, also causes acute hemorrhagic necrosis of tumors. Both TNF and IL-1 induce a cascade of events including the synthesis or release of each other. The present studies were thus undertaken to determine whether the hemorrhagic necrosis induced in tumors by IL-lα is due to TNF. Kinetic parameters of IL-lα-induced hemorrhage were similar to those observed with recombinant murine TNF-α (TNF-α) or LPS in RIF-1 fibrosarcomas in C3H/HeN (endotoxin-sensitive) mice. However, the amount of TNF found in the sera or tumors of animals treated with LPS was more than 20-fold higher than in mice treated with IL-lα, and LPS induced similar degrees of hemorrhagic necrosis, which was measured by determining the packed volume of red blood cells by Fe labeling. A low but significantly hemorrhagic dose of IL-lα induced no detectable TNF in tumors. Pretreatment with 250 μg of neutralizing antibody to TNF had no effect on IL-lα-induced hemorrhage, whereas TNF-α- and LPS-induced hemorrhagic effects were significantly reduced. These results demonstrate an important antitumor activity of IL-αa that appears to be independent of TNF. [J Natl Cancer Inst 83:842–848,1991] [ABSTRACT FROM PUBLISHER]

Published
1991

33. In Vivo Hematopoietic Effects of Recombinant Interleukin-lα in Mice: Stimulation of Granulocytic, Monocytic, Megakaryocytic, and Early Erythroid Progenitors, Suppression of Late-Stage Erythropoiesis, and Reversal of Erythroid Suppression With Erythropoietin

Author

Johnson, Candace S., Keckler, Douglas J., Topper, Maureen I., Braunschweiger, Paul G., and Furmanski, Philip

Abstract

lnterleukin-1 α (IL-1 α ) is a macrophage-derived, multifunctional cytokine that broadly potentiates myelopoiesis and induces the synthesis of hematopoietic colony-stimulating factors (CSF) in vitro and in vivo. To evaluate the possibility for use of IL-1 α in ameliorating in vivo bone marrow suppression induced by drugs or radiation, we examined the in vivo effects of the cytokine on erythropoietic and other hematopoietic progenitor cells. Normal mice were treated with a single intraperitoneal (IP) injection of recombinant human IL-1 αat varying doses and were assayed at various times post-treatment. By six hours postinjection, a significant suppression of mature erythroid progenitors (CFU-E) was observed in animals treated with IL-1 α (0.5 μg/mouse), with maximum suppression of CFU-E and peripheral blood reticulocyte counts occurring at 24 hours. Decreases in peripheral blood hematocrit did not occur after a single IL-1 α injection but were observed after multiple injections of the cytokine. The suppressive effects of IL-1 α on late-stage erythropoiesis were abrogated by simultaneous administration of erythropoietin (EPO). At 48 hours post-treatment, a marked stimulation was observed in the numbers of spleen and marrow immature erythroid (BFU-E), macrophage (CFU-M), granulocyte (CFU-G), gran-ulocyte-macrophage (CFU-GM), and megakaryocyte (CFU-meg) progenitor cells. These results demonstrate the potential use of IL-1 α as a generalized stimulator of hematopoiesis and show that the cytokine-induced suppression of late-stage erythropoiesis can be prevented by EPO.

Published
1989
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45. Acute Hemorrhagic Necrosis of Tumors Induced by Interleukin-1<IMG SRC="/math/alpha.gif" ALT="{alpha}" BORDER="0"> Effects Independent of Tumor Necrosis Factor

Author

Johnson, Candance S., Chang, Ming-jei, Braunschweiger, Paul G., and Furmanski, Philip

Abstract

Tumor necrosis factor (TNF), a protein synthesized in response to the endotoxin bacterial lipopolysaccharide (LPS), is the classical mediator of acute hemorrhagic necrosis of tumors. We have demonstrated that interleukin-la (IL-lα), with a spectrum of activities very similar to those of TNF, also causes acute hemorrhagic necrosis of tumors. Both TNF and IL-1 induce a cascade of events including the synthesis or release of each other. The present studies were thus undertaken to determine whether the hemorrhagic necrosis induced in tumors by IL-lα is due to TNF. Kinetic parameters of IL-lα-induced hemorrhage were similar to those observed with recombinant murine TNF-α (TNF-α) or LPS in RIF-1 fibrosarcomas in C3H/HeN (endotoxin-sensitive) mice. However, the amount of TNF found in the sera or tumors of animals treated with LPS was more than 20-fold higher than in mice treated with IL-lα, and LPS induced similar degrees of hemorrhagic necrosis, which was measured by determining the packed volume of red blood cells by 59Fe labeling. A low but significantly hemorrhagic dose of IL-lα induced no detectable TNF in tumors. Pretreatment with 250 μg of neutralizing antibody to TNF had no effect on IL-lα-induced hemorrhage, whereas TNF-α- and LPS-induced hemorrhagic effects were significantly reduced. These results demonstrate an important antitumor activity of IL-αa that appears to be independent of TNF. [J Natl Cancer Inst 83:842–848,1991]

Published
1991
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46. 2-deoxy-D-glucose increases the efficacy of adriamycin and paclitaxel in human osteosarcoma and non-small cell lung cancers in vivo.

Author

Maschek G, Savaraj N, Priebe W, Braunschweiger P, Hamilton K, Tidmarsh GF, De Young LR, and Lampidis TJ

Subjects
Animals, Bone Neoplasms pathology, Drug Synergism, Humans, Mice, Mice, Nude, Osteosarcoma pathology, Transplantation, Heterologous, Tumor Cells, Cultured, Bone Neoplasms drug therapy, Carcinoma, Non-Small-Cell Lung drug therapy, Deoxyglucose pharmacology, Doxorubicin toxicity, Lung Neoplasms drug therapy, Osteosarcoma drug therapy, Paclitaxel toxicity
Abstract

Slow-growing cell populations located within solid tumors are difficult to target selectively because most cells in normal tissues also have low replication rates. However, a distinguishing feature between slow-growing normal and tumor cells is the hypoxic microenvironment of the latter, which makes them extraordinarily dependent on anaerobic glycolysis for survival. Previously, we have shown that hypoxic tumor cells exhibit increased sensitivity to inhibitors of glycolysis in three distinct in vitro models. Based on these results, we predicted that combination therapy of a chemotherapeutic agent to target rapidly dividing cells and a glycolytic inhibitor to target slow-growing tumor cells would have better efficacy than either agent alone. Here, we test this strategy in vivo using the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) in combination with Adriamycin (ADR) or paclitaxel in nude mouse xenograft models of human osteosarcoma and non-small cell lung cancer. Nude mice implanted with osteosarcoma cells were divided into four groups as follows: (a) untreated controls; (b) mice treated with ADR alone; (c) mice treated with 2-DG alone; or (d) mice treated with a combination of ADR + 2-DG. Treatment began when tumors were either 50 or 300 mm(3) in volume. Starting with small or large tumors, the ADR + 2-DG combination treatment resulted in significantly slower tumor growth (and therefore longer survival) than the control, 2-DG, or ADR treatments (P < 0.0001). Similar beneficial effects of combination treatment were found with 2-DG and paclitaxel in the MV522 non-small cell lung cancer xenograft model. In summary, the treatment of tumors with both the glycolytic inhibitor 2-DG and ADR or paclitaxel results in a significant reduction in tumor growth compared with either agent alone. Overall, these results, combined with our in vitro data, provide a rationale for initiating clinical trials using glycolytic inhibitors in combination with chemotherapeutic agents to increase their therapeutic effectiveness.

Published
2004
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47. A Carbohydrate-Linked Cisplatin Analogue Having Antitumor Activity.

Author

Chen Y, Heeg MJ, Braunschweiger PG, Xie W, and Wang PG

Abstract

An unprotected and intact carbohydrate moiety has been observed for the first time in a transition metal complex. The carbohydrate-linked platinum(II) complex cis-dichloro[(2-β-D-glucopyranosidyl)propane-1,3-diamine]platinum (see picture) is an analogue of cisplatin and exhibits comparable antitumor activity along with increased solubility in water., (© 1999 WILEY-VCH Verlag GmbH, Weinheim, Fed. Rep. of Germany.)

Published
1999
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