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4. Contributors

Author

Abdurakhmanov, Alexander, primary, Abu-Shakra, Mahmoud, additional, Afanasyeva, Marina, additional, Agmon-Levin, Nancy, additional, Albert, Paul J., additional, Almeida, Isabel, additional, Alves, Rute, additional, Amital, Howard, additional, Andrade, Paulo, additional, Antonelli, Alessandro, additional, Puccetti, Antonio, additional, Arango, María-Teresa, additional, Atzeni, Fabiola, additional, Baird, Alison E., additional, Balbir-Gurman, Alexandra, additional, Bashi, Tomer, additional, Batticciotto, Alberto, additional, Benucci, Maurizio, additional, Blank, Miri, additional, Bogdanos, Dimitrios P., additional, Bombardieri, S., additional, Borella, E., additional, Bosis, Samantha, additional, Bournia, Vasiliki Kalliopi, additional, Brandão, Mariana, additional, Braun-Moscovici, Yolanda, additional, Brender-Gotlieb, Neta, additional, Cainelli, Francesca, additional, Caldas, Cezar Augusto Muniz, additional, Campar, A., additional, Carvalheiras, Graziela, additional, Cervera, R., additional, Chapman, Joab, additional, Chastain, Emily M.L., additional, Claudio, Lunardi, additional, Cohen, Eytan, additional, Conti, Fabrizio, additional, Correia, J., additional, Carvalho, Jozélio Freire de, additional, Rossa, A. Della, additional, Detrick, Barbara, additional, Deutsch, Melanie, additional, Di Domenicantonio, Andrea, additional, Domeneghetti, M., additional, Domingues, Vital, additional, Doria, A., additional, Dow, Coad Thomas, additional, Dreyfus, David H., additional, Drouin, Elise E., additional, Dubaniewicz, Anna, additional, Durai, Malarvizhi, additional, Ebringer, Alan, additional, Ehrenfeld, Michael, additional, Elisa, Tinazzi, additional, Esposito, Susanna, additional, Fallahi, Poupak, additional, Faria, Raquel, additional, Farinha, Fátima, additional, Ferrannini, Ele, additional, Ferrari, Silvia Martina, additional, Ferreira, Alvaro, additional, Ferrão, C., additional, Garg, Ravindra Kumar, additional, Gatto, M., additional, Ghirardello, A., additional, Giovanna, Zanoni, additional, Giuseppe, Patuzzo, additional, Givaty, Gili, additional, Guilherme, Luiza, additional, Hammerstad, Sara Salehi, additional, Hodak, Emillia, additional, Hooks, John J., additional, Iaccarino, L., additional, Invernizzi, Pietro, additional, Israeli, Eitan, additional, Jamin, Christophe, additional, Janket, Sok-Ja, additional, Jarčuška, Peter, additional, Jones, Rodney P., additional, Kalil, Jorge, additional, Kanasi, Eleni, additional, Kivity, Shaye, additional, Konikoff, Tom, additional, Kozáková, D., additional, Krause, Ilan, additional, Lerner, Aaron, additional, Lidar, Merav, additional, Ling, Eduard, additional, Mahajna, Hussein, additional, Mahroum, Naim, additional, Maoz-Segal, Ramit, additional, Marinho, António, additional, Marshall, Trevor G., additional, Martinelli, Maria, additional, Marzia, Dolcino, additional, Mavragani, Clio P., additional, Mendonça, Teresa, additional, Miller, Stephen D., additional, Mimouni, Daniel, additional, Monteiro, Marta, additional, Moudgil, Kamal D., additional, Moulton, Vaishali R., additional, Moutsopoulos, Haralampos M., additional, Nagpal, Kamalpreet, additional, Neves, Esmeralda, additional, Nussenblatt, Robert, additional, Ollech, Ayelet, additional, Palma, L., additional, Pasoto, Sandra Gofinet, additional, Pella, Daniel, additional, Pereira, Cláudia, additional, Perricone, Carlo, additional, Petríková, Jana, additional, Proal, Amy D., additional, Rashid, Taha, additional, Reif, Shimon, additional, Renaudineau, Yves, additional, Ribeiro, Francinne Machado, additional, Rigante, Donato, additional, Rigopoulou, Eirini I., additional, Rose, Noel R., additional, Rosário, Cristina, additional, Rovenský, J., additional, Sakkas, Lazaros I., additional, Sarzi-Puttini, Piercarlo, additional, Seguro, Luciana Parente Costa, additional, Semino, Margherita, additional, Shoenfeld, Yehuda, additional, Silva, S., additional, Simonin, Laurent, additional, Smyk, Daniel S., additional, Sousa, Rita Catarina Medeiros, additional, Stagnaro, C., additional, Steere, Allen C., additional, Strle, Klemen, additional, Tektonidou, Maria G., additional, Tishler, Moshe, additional, Tomer, Yaron, additional, Toubi, Elias, additional, Tsokos, George C., additional, Vadasz, Zahava, additional, Valesini, Guido, additional, Vasconcelos, Carlos, additional, Vasconcelos, Júlia, additional, Vassilopoulos, Dimitrios, additional, Venkatesha, Shivaprasad H., additional, Vento, Sandro, additional, Viale, Christophe, additional, Villanueva, Ronald, additional, Vita, Pedro, additional, Wilson, Clyde, additional, Youinou, Pierre, additional, Záňová, E., additional, Zandman-Goddard, Gisele, additional, and Zen, M., additional

Published
2015
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8. Vitamin D discovery outpaces FDA decision making

Author

Marshall, Trevor G.

Subjects
United States. Food and Drug Administration -- Laws, regulations and rules, Obesity -- Diet therapy, Alfacalcidol -- Nutritional aspects, Alfacalcidol -- Laws, regulations and rules, Calcifediol -- Nutritional aspects, Calcifediol -- Laws, regulations and rules, Vitamin D -- Nutritional aspects, Vitamin D -- Laws, regulations and rules, Government regulation, Biological sciences
Abstract

Research findings that extensive use of vitamin D as a food supplement provides only short-term advantage, while future generations are likely to suffer from an epidemic expansion of obesity and chronic diseases are presented. It is suggested that the role of vitamin D must be reexamined by the FDA and its recommendation to expand addition of Vitamin D to foods must be curtailed.

Published
2008

14. Are statins analogues of vitamin D?

Author

Hiemstra, Thomas F., Gonzalez-Clemente, Jose-Miguel, Gimenez-Palop, Olga, Vilardell, Carme, Caixas, Assumpta, Gimenez-Perez, Gabriel, Li, Hai-feng, Marshall, Trevor G., and Grimes, David

Published
2006

24. Letters.

Author

Woodburn, Bruce D., Bonisteel, Paul, Lofsky, Stanley, Hill, Michael D., Naglie, Gary, Goldlist, Barry, Etchells, Ed, Tomlinson, George, Prigent, Bernard M., Lexchin, Joel, Spence, J. David, Oakley, Jr., Godfrey P., Van den Hof, Michiel C., Persad, Vidia L., Marshall, Trevor G., Hanley, David A., and Majeed, Azeem

Subjects
LETTERS to the editor, FAMILY medicine, MEDICAL care for older people, DRUG interactions
Abstract

Presents letters on medical subjects as of October 15, 2002. Reactions to previous article on the decline of family medicine; Evidence of parallel problems with stroke care and postoperative care for geriatric patients with hip fractures; Interaction of certain drugs and grapefruit; Importance of folic acid fortification; Other issues.

Published
2002

26. The Magnificent Seven: The Premiers and Prime Ministers of Barbados, 1946-2006.

Author

Marshall, Trevor G.

Abstract

Information for tourists on the premiers and prime ministers of Barbados from 1946 to 2006, from a chapter of the book "Barbados: Experience the Authentic Caribbean" is presented. Sir Grantley Herbert Adams was considered as Father of Political Democracy and Father of Franchise Reform. Doctor Hugh Gordon Hylvester Cummings served as Premier of Barbados from 1958 to 1961. Errol Walton Barrow served as prime minister from 1966 to 1976 and from May 1986 to June 1987.

Published
2007

27. Caribbean Eye. Tape 6, Barbados.

Author

Banyan Archives, production company, publisher., Gabby (Calypso musician), performer., Marshall, Trevor G., interviewee., and Antrobus, Peggy, speaker.

Published
1990

28. Re-framing the theory of autoimmunity in the era of the microbiome: persistent pathogens, autoantibodies, and molecular mimicry.

Author

Proal AD and Marshall TG

Subjects
Dysbiosis immunology, Dysbiosis microbiology, Humans, Autoantibodies immunology, Autoimmunity, Microbiota, Models, Immunological, Molecular Mimicry immunology
Abstract

The theory of autoimmunity was developed at a time when the human body was regarded as largely sterile. Antibodies in patients with chronic inflammatory disease could consequently not be tied to persistent human pathogens. The concept of the "autoantibody" was created to reconcile this phenomenon. Today, however, the discovery of the human microbiome has revolutionized our understanding of human biology. Humans are superorganisms that harbor trillions of persistent microbial cells. Indeed, vast human microbiomes have been detected in human tissue and blood. These microbial ecosystems harbor thousands of newly identified bacteria, viruses, and other microorganisms -- most of which can act as pathogens under conditions of immunosuppression. The theory of autoimmunity must be revised to account for the human microbiome. Here, we propose a model in which "autoantibodies" are created in response to chronic, persistent microbiome pathogens. The structural homology (molecular mimicry) between pathogen and host proteins can result in "collateral damage" to surrounding human tissue. This calls for a paradigm shift in autoimmune disease treatment. Immunosuppressive medications palliate inflammatory symptoms at the expense of microbiome health and balance. In contrast, treatments that support the immune system in autoimmune disease could allow patients to target pathogens at the root of the disease process.

Published
2018

29. Microbe-microbe and host-microbe interactions drive microbiome dysbiosis and inflammatory processes.

Author

Proal AD, Lindseth IA, and Marshall TG

Subjects
Animals, Dysbiosis immunology, Dysbiosis virology, Gastrointestinal Microbiome immunology, Host-Pathogen Interactions, Humans, Inflammation metabolism, Dysbiosis microbiology, Microbiota physiology
Abstract

An extensive microbiome comprised of bacteria, viruses, bacteriophages, and fungi is now understood to persist in nearly every human body site, including tissue and blood. The genomes of these microbes continually interact with the human genome in order to regulate host metabolism. Many components of this microbiome are capable of both commensal and pathogenic activity. They are additionally able to persist in both 'acute' and chronic forms. Inflammatory conditions historically studied separately (autoimmune, neurological and malignant) are now repeatedly tied to a common trend: imbalance or dysbiosis of these microbial ecosystems. Population-based studies of the microbiome can shed light on this dysbiosis. However, it is the collective activity of the microbiome that drives inflammatory processes via complex microbe-microbe and host-microbe interactions. Many microbes survive as polymicrobial entities in order to evade the immune response. Pathogens in these communities alter their gene expression in ways that promote community-wide virulence. Other microbes persist inside the cells of the immune system, where they directly interfere with host transcription, translation, and DNA repair mechanisms. The numerous proteins and metabolites expressed by these pathogens further dysregulate human gene expression in a manner that promotes imbalance and immunosuppression. Molecular mimicry, or homology between host and microbial proteins, complicates the nature of this interference. When taken together, these microbe-microbe and host-microbe interactions are capable of driving the large-scale failure of human metabolism characteristic of many different inflammatory conditions.

Published
2017

30. Inflammatory disease and the human microbiome.

Author

Proal AD, Albert PJ, and Marshall TG

Subjects
Gene Expression Regulation, Bacterial, Genome, Human, Genomics, Humans, Immunity, Innate, Metagenome, Inflammation microbiology, Inflammation physiopathology, Microbiota
Abstract

The human body is a superorganism in which thousands of microbial genomes continually interact with the human genome. A range of physical and neurological inflammatory diseases are now associated with shifts in microbiome composition. Seemingly disparate inflammatory conditions may arise from similar disruption of microbiome homeostasis. Intracellular pathogens long associated with inflammatory disease are able to slow the innate immune response by dysregulating activity of the VDR nuclear receptor. This facilitates the ability of other species to gradually accumulate in tissue and blood, where they generate proteins and metabolites that significantly interfere with the body's metabolic processes. The microbes that contribute to this dysfunction are often inherited from family members. Immunosuppressive therapies for inflammatory disease allow pathogens driving these processes to spread with greater ease. In contrast to immunosuppression, treatments that stimulate the immune system seem to allow for reversal of this pathogen-induced genomic dysregulation.

Published
2014

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