Search

Your search keyword '"Nero, Thomas"' showing total 31 results
Start Over Author "Nero, Thomas"
31 results on '"Nero, Thomas"'

2. Self-administered intranasal etripamil using a symptom-prompted, repeat-dose regimen for atrioventricular-nodal-dependent supraventricular tachycardia (RAPID): a multicentre, randomised trial

Author

Ip, James E, Jones, Alonzo, Sr, Stambler, Bruce S, Schleinkofer, David E, Winters, Stephen, Lam, Wilson, Goldstein, Robert, Dor, Isaac Dor, Talwar, Sandeep, O'Neill, Padraig G, Koren, Michael J, Beinart, Sean C, Ambati, Srivani, Mazer, Sean P, Kinn, Robert M, Roy, Karine, Manshadi, Ramin, Kuk, Richard, Verma, Aditya, Phelan, Timothy, Stoian, Alexandru A, Ellenbogen, Kenneth, Jayachandran, J Vijay, Connelly, Terence P, Daccarett, Marcos, Gandhi, Gaurang, Mittal, Suneet, Abdel-Wahab, Amir, Augostini, Ralph, Ip, John H, Sorrentino, Denise, Roux, Jean-Francois, Brar, Ramandeep, Khoo, Clarence, Bennett, Matthew, Lo, Eric, Coutu, Benoit, Sterns, Laurence, Greer, Gerald S, Gujja, Pradeep, Gianfagna, Robert A, Swarup, Vijendra, Sogade, Felix, Wilton, Stephen, Ruisi, Christopher, Barbera, Saverio, Banchs, Javier E., Korley, Victoria, Schulze, Christopher, Damle, Roger, Healey, Jeffrey Sean, Pandey, A Shekhar, Anderson, Jeffrey L, Venkatachalam, K L, Noseworthy, Peter, Mondésert, Blandine, Verma, Atul, Friars, Douglas G, Kambur, Thomas R, Lockwood, Evan, Meininger, Glenn, Olsovsky, Greg, Jones Sr, Alonzo, Greer, Gerald, Mehta, Rohit, Akbar, Saleem, Salman, Malik, Rama, Bhola, Arora, Ramesh, Shah, Dhirenkumar, Shah, Rakesh, Cammarata, Michael, Owens, Andrew, Ludington, Katherine, Wharton, Marcus, Bagheri, Michael, Khan, Mohammed, Carr, Kenneth Warren, Siddique, Sultan, Parvathaneni, Sunthosh, Devabhaktuni, Subodh, Mouhaffel, Assad, Mark, George, Di Biase, Luigi, Rangappa, Sunil, Morton, Jared, Yarmohammadi, Hirad, Karim, Amin, Martinez Fleites, Aldo, Nero, Thomas, Shafiq, Qaiser, Pandey, Shekhar, Khaykin, Yaariv, Joza, Jacqueline, Gosselin, Gilbert, Skanes, Allen, Vyselaar, John, Savard, Daniel, Heidbuchel, Hein, Xhaet, Olivier, Catez, Emmanuel, Vijgen, Johan, Godart, Pascal, Casado, Ruben, Mairesse, Georges, Rossenbacker, Tom, Haemers, Peter, Hoffer, Etienne, Hausman, Pierre, Vertes, Andras, Duray, Gabor, Szolnoki, Erzsebet, Csanadi, Zoltan, Lakatos, Ferenc, Alings, Marco, Dorman, Reinhart, Tuininga, Y S, Jansen, W, Velthuis, Sebastiaan, van Bemmel, B, Bech, Gerhard Jan Willem, Pisters, Ron, Valk, Suzanne, Romer, Tjeerd, Luermans, Justin, Beelen, Driek, van Eck, Martijn, Houtgraaf, Jaco, Vet, Thijs, Shellings, Dirk, Oosterhof, T, Miekus, Pawel, Bebenek, Waldemar, Bielecka-Dabrowa, Agata, Gniot, Jacek, Zmuda, Witold, Kasprzak, Michal, Balak, Wojciech, Ptaszynski, Pawel, Nowak, Jacek, Prokopczuk, Janusz, Przybylski, Andrzej, Wozniak-Skowerska, Iwona, Derejko, Pawel, Czarnecka, Danuta, Janas, Adam, Merino Llorens, Jose Luis, Tercedor, Luis, Iniguez Romo, Andres, Ruiz Granell, Ricardo, Gonzalez Juanatey, Jose Ramon, Pascual-Figal, Domingo, Martinez-Selles, Manuel, Anguera Camos, Ignacio, Ibanez Criado, Alicia, Matrinez Basterra, Javier, Izquierdo, Alvaro, Rivas Gandara, Nuria, Alegret Colome, Josep M, Perez Diez, Diego, Martínez Hervás, Miguel Ángel, Medina, Maria, Segura Saint-Gerons, Jose María, Pedrote Leal, Alonso, Fernandez Lozano, Ignacio, Quesada, Aurelio, Guerra Ramos, Jose, Sarrias, Axel, Ramos Maqueda, Javier, Mansourati, Jacques, Defaye, Pascal, Guedon-Moreau, Laurence, Milhem, Antoine, De Guillebon, Maxime, Chevalier, Philippe, Badoz, Marc, Kriatselis, Charalampos, Simonis, Gregor, Lewalter, Thorsten, Zarse, Markus, Wilke, Andreas, Kraemer, Fabian, Al-Zoebi, Ayham, Camm, A John, Dorian, Paul, Kowey, Peter R, Merino, Jose L, Piccini, Jonathan P, Pokorney, Sean D, Sager, Philip T, Wharton, J Marcus, Bharucha, David B, Plat, Francis, Shardonofsky, Silvia, and Chen, Michael

Published
2023
Full Text
View/download PDF

4. Self-administered intranasal etripamil using a symptom-prompted, repeat-dose regimen for atrioventricular-nodal-dependent supraventricular tachycardia (RAPID): a multicentre, randomised trial

Author

Stambler, Bruce S, primary, Camm, A John, additional, Alings, Marco, additional, Dorian, Paul, additional, Heidbuchel, Hein, additional, Houtgraaf, Jaco, additional, Kowey, Peter R, additional, Merino, Jose L, additional, Mondésert, Blandine, additional, Piccini, Jonathan P, additional, Pokorney, Sean D, additional, Sager, Philip T, additional, Verma, Atul, additional, Wharton, J Marcus, additional, Bharucha, David B, additional, Plat, Francis, additional, Shardonofsky, Silvia, additional, Chen, Michael, additional, Ip, James E, additional, Jones, Alonzo, additional, Stambler, Bruce S, additional, Schleinkofer, David E, additional, Winters, Stephen, additional, Lam, Wilson, additional, Goldstein, Robert, additional, Dor, Isaac Dor, additional, Talwar, Sandeep, additional, O'Neill, Padraig G, additional, Koren, Michael J, additional, Beinart, Sean C, additional, Ambati, Srivani, additional, Mazer, Sean P, additional, Kinn, Robert M, additional, Roy, Karine, additional, Manshadi, Ramin, additional, Kuk, Richard, additional, Verma, Aditya, additional, Phelan, Timothy, additional, Stoian, Alexandru A, additional, Ellenbogen, Kenneth, additional, Jayachandran, J Vijay, additional, Connelly, Terence P, additional, Daccarett, Marcos, additional, Gandhi, Gaurang, additional, Mittal, Suneet, additional, Abdel-Wahab, Amir, additional, Augostini, Ralph, additional, Ip, John H, additional, Sorrentino, Denise, additional, Roux, Jean-Francois, additional, Brar, Ramandeep, additional, Khoo, Clarence, additional, Bennett, Matthew, additional, Lo, Eric, additional, Coutu, Benoit, additional, Sterns, Laurence, additional, Greer, Gerald S, additional, Gujja, Pradeep, additional, Gianfagna, Robert A, additional, Swarup, Vijendra, additional, Sogade, Felix, additional, Wilton, Stephen, additional, Ruisi, Christopher, additional, Barbera, Saverio, additional, Banchs, Javier E., additional, Korley, Victoria, additional, Schulze, Christopher, additional, Damle, Roger, additional, Healey, Jeffrey Sean, additional, Pandey, A Shekhar, additional, Anderson, Jeffrey L, additional, Venkatachalam, K L, additional, Noseworthy, Peter, additional, Friars, Douglas G, additional, Kambur, Thomas R, additional, Lockwood, Evan, additional, Meininger, Glenn, additional, Olsovsky, Greg, additional, Jones Sr, Alonzo, additional, Greer, Gerald, additional, Mehta, Rohit, additional, Akbar, Saleem, additional, Salman, Malik, additional, Rama, Bhola, additional, Arora, Ramesh, additional, Shah, Dhirenkumar, additional, Shah, Rakesh, additional, Cammarata, Michael, additional, Owens, Andrew, additional, Ludington, Katherine, additional, Wharton, Marcus, additional, Bagheri, Michael, additional, Khan, Mohammed, additional, Carr, Kenneth Warren, additional, Siddique, Sultan, additional, Parvathaneni, Sunthosh, additional, Devabhaktuni, Subodh, additional, Mouhaffel, Assad, additional, Mark, George, additional, Di Biase, Luigi, additional, Rangappa, Sunil, additional, Morton, Jared, additional, Yarmohammadi, Hirad, additional, Karim, Amin, additional, Martinez Fleites, Aldo, additional, Nero, Thomas, additional, Shafiq, Qaiser, additional, Pandey, Shekhar, additional, Khaykin, Yaariv, additional, Joza, Jacqueline, additional, Gosselin, Gilbert, additional, Skanes, Allen, additional, Vyselaar, John, additional, Savard, Daniel, additional, Xhaet, Olivier, additional, Catez, Emmanuel, additional, Vijgen, Johan, additional, Godart, Pascal, additional, Casado, Ruben, additional, Mairesse, Georges, additional, Rossenbacker, Tom, additional, Haemers, Peter, additional, Hoffer, Etienne, additional, Hausman, Pierre, additional, Vertes, Andras, additional, Duray, Gabor, additional, Szolnoki, Erzsebet, additional, Csanadi, Zoltan, additional, Lakatos, Ferenc, additional, Dorman, Reinhart, additional, Tuininga, Y S, additional, Jansen, W, additional, Velthuis, Sebastiaan, additional, van Bemmel, B, additional, Bech, Gerhard Jan Willem, additional, Pisters, Ron, additional, Valk, Suzanne, additional, Romer, Tjeerd, additional, Luermans, Justin, additional, Beelen, Driek, additional, van Eck, Martijn, additional, Vet, Thijs, additional, Shellings, Dirk, additional, Oosterhof, T, additional, Miekus, Pawel, additional, Bebenek, Waldemar, additional, Bielecka-Dabrowa, Agata, additional, Gniot, Jacek, additional, Zmuda, Witold, additional, Kasprzak, Michal, additional, Balak, Wojciech, additional, Ptaszynski, Pawel, additional, Nowak, Jacek, additional, Prokopczuk, Janusz, additional, Przybylski, Andrzej, additional, Wozniak-Skowerska, Iwona, additional, Derejko, Pawel, additional, Czarnecka, Danuta, additional, Janas, Adam, additional, Merino Llorens, Jose Luis, additional, Tercedor, Luis, additional, Iniguez Romo, Andres, additional, Ruiz Granell, Ricardo, additional, Gonzalez Juanatey, Jose Ramon, additional, Pascual-Figal, Domingo, additional, Martinez-Selles, Manuel, additional, Anguera Camos, Ignacio, additional, Ibanez Criado, Alicia, additional, Matrinez Basterra, Javier, additional, Izquierdo, Alvaro, additional, Rivas Gandara, Nuria, additional, Alegret Colome, Josep M, additional, Perez Diez, Diego, additional, Martínez Hervás, Miguel Ángel, additional, Medina, Maria, additional, Segura Saint-Gerons, Jose María, additional, Pedrote Leal, Alonso, additional, Fernandez Lozano, Ignacio, additional, Quesada, Aurelio, additional, Guerra Ramos, Jose, additional, Sarrias, Axel, additional, Ramos Maqueda, Javier, additional, Mansourati, Jacques, additional, Defaye, Pascal, additional, Guedon-Moreau, Laurence, additional, Milhem, Antoine, additional, De Guillebon, Maxime, additional, Chevalier, Philippe, additional, Badoz, Marc, additional, Kriatselis, Charalampos, additional, Simonis, Gregor, additional, Lewalter, Thorsten, additional, Zarse, Markus, additional, Wilke, Andreas, additional, Kraemer, Fabian, additional, and Al-Zoebi, Ayham, additional

Published
2023
Full Text
View/download PDF

9. The Thr300Ala variant in ATG16L1 is associated with improved survival in human colorectal cancer and enhanced production of type I interferon

Author

Grimm, Wesley A, Messer, Jeannette S, Murphy, Stephen F, Nero, Thomas, Lodolce, James P, Weber, Christopher R, Logsdon, Mark F, Bartulis, Sarah, Sylvester, Brooke E, Springer, Amanda, Dougherty, Urszula, Niewold, Timothy B, Kupfer, Sonia S, Ellis, Nathan, Huo, Dezheng, Bissonnette, Marc, and Boone, David L

Published
2016
Full Text
View/download PDF

11. Social evolution of shared biofilm matrix components.

Author

Jung-Shen B. Tai, Mukherjee, Saikat, Nero, Thomas, Olson, Rich, Tithof, Jeffrey, Nadell, Carey D., and Jing Yan

Subjects
SOCIAL evolution, BIOFILMS, EXTRACELLULAR matrix proteins, IMMOBILIZED proteins, VIBRIO cholerae
Abstract

Biofilm formation is an important and ubiquitous mode of growth among bacteria. Central to the evolutionary advantage of biofilm formation is cell-cell and cell-surface adhesion achieved by a variety of factors, some of which are diffusible compounds that may operate as classical public goods--factors that are costly to produce but may benefit other cells. An outstanding question is how diffusible matrix production, in general, can be stable over evolutionary timescales. In this work, using Vibrio cholerae as a model, we show that shared diffusible biofilm matrix proteins are indeed susceptible to cheater exploitation and that the evolutionary stability of producing these matrix components fundamentally depends on biofilm spatial structure, intrinsic sharing mechanisms of these components, and flow conditions in the environment. We further show that exploitation of diffusible adhesion proteins is localized within a well-defined spatial range around cell clusters that produce them. Based on this exploitation range and the spatial distribution of cell clusters, we constructed a model of costly diffusible matrix production and related these length scales to the relatedness coefficient in social evolution theory. Our results show that production of diffusible biofilm matrix components is evolutionarily stable under conditions consistent with natural biofilm habitats and host environments. We expect the mechanisms revealed in this study to be relevant to other secreted factors that operate as cooperative public goods in bacterial communities and the concept of exploitation range and the associated analysis tools to be generally applicable. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

14. Yersinia pestis targets neutrophils via complement receptor 3

Author

Merritt, Peter M., Nero, Thomas, Bohman, Lesley, Felek, Suleyman, Krukonis, Eric S., and Marketon, Melanie M.

Subjects
Mice, Neutrophils, Yersinia pestis, Animals, Macrophage-1 Antigen, Article, Cells, Cultured, Endocytosis
Abstract

Yersinia species display a tropism for lymphoid tissues during infection, and the bacteria select innate immune cells for delivery of cytotoxic effectors by the type III secretion system. Yet, the mechanism for target cell selection remains a mystery. Here we investigate the interaction of Yersinia pestis with murine splenocytes to identify factors that participate in the targeting process. We find that interactions with primary immune cells rely on multiple factors. First, the bacterial adhesin Ail is required for efficient targeting of neutrophils in vivo. However, Ail does not appear to directly mediate binding to a specific cell type. Instead, we find that host serum factors direct Y. pestis to specific innate immune cells, particularly neutrophils. Importantly, specificity towards neutrophils was increased in the absence of bacterial adhesins because of reduced targeting of other cell types, but this phenotype was only visible in the presence of mouse serum. Addition of antibodies against complement receptor 3 and CD14 blocked target cell selection, suggesting that a combination of host factors participate in steering bacteria towards neutrophils during plague infection.

Published
2014

15. The Thr300Ala variant in ATG16L1 is associated with improved survival in human colorectal cancer and enhanced production of type I interferon

Author

Grimm, Wesley A, primary, Messer, Jeannette S, additional, Murphy, Stephen F, additional, Nero, Thomas, additional, Lodolce, James P, additional, Weber, Christopher R, additional, Logsdon, Mark F, additional, Bartulis, Sarah, additional, Sylvester, Brooke E, additional, Springer, Amanda, additional, Dougherty, Urszula, additional, Niewold, Timothy B, additional, Kupfer, Sonia S, additional, Ellis, Nathan, additional, Huo, Dezheng, additional, Bissonnette, Marc, additional, and Boone, David L, additional

Published
2015
Full Text
View/download PDF

17. Intestinal epithelial expression of TNFAIP3 results in microbial invasion of the inner mucus layer and induces colitis in IL-10-deficient mice

Author

Murphy, Stephen F., primary, Rhee, Lesley, additional, Grimm, Wesley A., additional, Weber, Christopher R., additional, Messer, Jeannette S., additional, Lodolce, James P., additional, Chang, Jonathan E., additional, Bartulis, Sarah J., additional, Nero, Thomas, additional, Kukla, Renata A., additional, MacDougall, Gordon, additional, Binghay, Charles, additional, Kolodziej, Lauren E., additional, and Boone, David L., additional

Published
2014
Full Text
View/download PDF

20. Expression of TNFAIP3 in intestinal epithelial cells protects from DSS- but not TNBS-induced colitis

Author

Rhee, Lesley, primary, Murphy, Stephen F., additional, Kolodziej, Lauren E., additional, Grimm, Wesley A., additional, Weber, Christopher R., additional, Lodolce, James P., additional, Chang, Jonathan E., additional, Bartulis, Sarah J., additional, Messer, Jeannette S., additional, Schneider, Jeff R., additional, Paski, Shirley, additional, Nero, Thomas M., additional, and Boone, David L., additional

Published
2012
Full Text
View/download PDF

23. Y ersinia pestis targets neutrophils via complement receptor 3.

Author

Merritt, Peter M., Nero, Thomas, Bohman, Lesley, Felek, Suleyman, Krukonis, Eric S., and Marketon, Melanie M.

Subjects
*YERSINIA pestis, *NEUTROPHILS, *COMPLEMENT receptors, *CD14 antigen, *PLAGUE
Abstract

Yersinia species display a tropism for lymphoid tissues during infection, and the bacteria select innate immune cells for delivery of cytotoxic effectors by the type III secretion system. Yet, the mechanism for target cell selection remains a mystery. Here we investigate the interaction of Y ersinia pestis with murine splenocytes to identify factors that participate in the targeting process. We find that interactions with primary immune cells rely on multiple factors. First, the bacterial adhesin Ail is required for efficient targeting of neutrophils in vivo. However, Ail does not appear to directly mediate binding to a specific cell type. Instead, we find that host serum factors direct Y . pestis to specific innate immune cells, particularly neutrophils. Importantly, specificity towards neutrophils was increased in the absence of bacterial adhesins because of reduced targeting of other cell types, but this phenotype was only visible in the presence of mouse serum. Addition of antibodies against complement receptor 3 and CD14 blocked target cell selection, suggesting that a combination of host factors participate in steering bacteria towards neutrophils during plague infection. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

28. Intestinal epithelial expression of TNFAIP3 results in microbial invasion of the inner mucus layer and induces colitis in IL-10-deficient mice.

Author

Murphy SF, Rhee L, Grimm WA, Weber CR, Messer JS, Lodolce JP, Chang JE, Bartulis SJ, Nero T, Kukla RA, MacDougall G, Binghay C, Kolodziej LE, and Boone DL

Subjects
Animals, Antigens, Neoplasm genetics, Antigens, Neoplasm metabolism, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Colitis, Ulcerative genetics, Colitis, Ulcerative microbiology, Cysteine Endopeptidases genetics, Gene Deletion, Intestinal Mucosa microbiology, Intestinal Mucosa pathology, Intracellular Signaling Peptides and Proteins genetics, Lectins, C-Type genetics, Lectins, C-Type metabolism, Mice, Mice, Inbred C57BL, Pancreatitis-Associated Proteins, Ribonuclease, Pancreatic genetics, Ribonuclease, Pancreatic metabolism, Tumor Necrosis Factor alpha-Induced Protein 3, Colitis, Ulcerative metabolism, Cysteine Endopeptidases metabolism, Interleukin-10 genetics, Intestinal Mucosa metabolism, Intracellular Signaling Peptides and Proteins metabolism, Microbiota
Abstract

Tumor necrosis factor-induced protein 3 (TNFAIP3; also known as A20) negatively regulates NF-κB and MAPK signals to control inflammatory responses. TNFAIP3 also protects against TNF-induced cell death. Intestinal epithelial cell (IEC) expression of TNFAIP3 improves barrier function and tight junction integrity and prevents dextran sulfate sodium (DSS)-induced IEC death and colitis. We therefore investigated the effects of TNFAIP3 expression in IEC on immune homeostasis in the intestines of immune-compromised mice. Villin-TNFAIP3 (v-TNFAIP3) transgenic mice were interbred with IL-10(-/-) mice (v-TNFAIP3 × IL-10(-/-)) and incidence, onset, and severity of colitis was assessed. v-TNFAIP3 × IL-10(-/-) mice displayed severe, early onset, and highly penetrant colitis that was not observed in IL-10(-/-) or v-TNFAIP3 mice. V-TNFAIP3 mice displayed altered expression of mucosal cytokines, increased numbers of mucosal regulatory T cells, and altered expression of mucosal antimicrobial peptides (AMPs). Microbial colonization of the inner mucus layer of v-TNFAIP3 mice was observed, along with alterations in the microbiome, but this was not sufficient to induce colitis in v-TNFAIP3 mice. The relative sterility of the inner mucus layer observed in wild-type and IL-10(-/-) mice was lost in v-TNFAIP3 × IL-10(-/-) mice. Thus IEC-derived factors, induced by signals that are inhibited by TNFAIP3, suppress the onset of inflammatory bowel disease in IL-10(-/-) mice. Our results indicate that IEC expression of TNFAIP3 alters AMP expression and allows microbial colonization of the inner mucus layer, which activates an IL-10-dependent anti-inflammatory process that is necessary to prevent colitis., (Copyright © 2014 the American Physiological Society.)

Published
2014
Full Text
View/download PDF

29. Expression of TNFAIP3 in intestinal epithelial cells protects from DSS- but not TNBS-induced colitis.

Author

Rhee L, Murphy SF, Kolodziej LE, Grimm WA, Weber CR, Lodolce JP, Chang JE, Bartulis SJ, Messer JS, Schneider JR, Paski S, Nero TM, and Boone DL

Subjects
Animals, Apoptosis drug effects, Colitis chemically induced, Cytokines biosynthesis, Intestinal Mucosa drug effects, Mice, Mice, Transgenic, NF-kappa B metabolism, Severity of Illness Index, Tumor Necrosis Factor alpha-Induced Protein 3, Colitis metabolism, Cysteine Endopeptidases metabolism, Dextran Sulfate adverse effects, Intestinal Mucosa metabolism, Intracellular Signaling Peptides and Proteins metabolism, Trinitrobenzenesulfonic Acid toxicity
Abstract

Intestinal epithelial cells (IEC) maintain gastrointestinal homeostasis by providing a physical and functional barrier between the intestinal lumen and underlying mucosal immune system. The activation of NF-κB and prevention of apoptosis in IEC are required to maintain the intestinal barrier and prevent colitis. How NF-κB activation in IEC prevents colitis is not fully understood. TNFα-induced protein 3 (TNFAIP3) is a NF-κB-induced gene that acts in a negative-feedback loop to inhibit NF-κB activation and also to inhibit apoptosis; therefore, we investigated whether TNFAIP3 expression in the intestinal epithelium impacts susceptibility of mice to colitis. Transgenic mice expressing TNFAIP3 in IEC (villin-TNFAIP3 Tg mice) were exposed to dextran sodium sulfate (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS), and the severity and characteristics of mucosal inflammation and barrier function were compared with wild-type mice. Villin-TNFAIP3 Tg mice were protected from DSS-induced colitis and displayed reduced production of NF-κB-dependent inflammatory cytokines. Villin-TNFAIP3 Tg mice were also protected from DSS-induced increases in intestinal permeability and induction of IEC death. Villin-TNFAIP3 Tg mice were not protected from colitis induced by TNBS. These results indicate that TNFAIP3 expression in IEC prevents colitis involving DSS-induced IEC death, but not colitis driven by T cell-mediated inflammation. As TNFAIP3 inhibits NF-κB activation and IEC death, expression of TNFAIP3 in IEC may provide an avenue to inhibit IEC NF-κB activation without inducing IEC death and inflammation.

Published
2012
Full Text
View/download PDF

30. Treatment of coronary aneurysm in acute myocardial infarction with AngioJet thrombectomy and JoStent coronary stent graft.

Author

Lee MS, Nero T, Makkar RR, and Wilentz JR

Subjects
Acute Disease, Coronary Aneurysm etiology, Humans, Male, Middle Aged, Myocardial Infarction therapy, Thrombectomy instrumentation, Angioplasty, Balloon, Coronary adverse effects, Coronary Aneurysm therapy, Myocardial Infarction complications, Stents, Thrombectomy methods
Abstract

A 54-year-old male with a history of coronary artery disease with a percutaneous transluminal coronary angioplasty and stenting presented to the emergency with an acute myocardial infarction. The patient underwent angiography which showed in-stent thrombosis of the right coronary artery along with 2 aneurysms proximal to the lesion. The right coronary artery was treated with AngioJet rheolytic thrombectomy and the JoStent coronary stent graft. To our knowledge, this is the first report of the use of the AngioJet rheolytic thrombectomy and the JoStent coronary stent graft in acute myocardial infarction.

Published
2004

31. Cutting balloon angioplasty.

Author

Lee MS, Singh V, Nero TJ, and Wilentz JR

Subjects
Coronary Stenosis therapy, Humans, Randomized Controlled Trials as Topic, Treatment Outcome, United States, Angioplasty, Balloon, Coronary methods, Angioplasty, Balloon, Coronary trends
Abstract

The Cutting Balloon is a unique angioplasty device used in percutaneous coronary interventions. The advantage of the Cutting Balloon is its ability to reduce vessel stretch and vessel injury by scoring the vessel longitudinally rather than causing an uncontrolled disruption of the atherosclerotic plaque. The atherotomes deliver a controlled fault line during dilatation to ensure that the crack propagation ensues in an orderly fashion. Lower balloon inflation pressures (4 8 atmospheres) are recommended with the Cutting Balloon. The Cutting Balloon also dilates the target vessel with less force to decrease the risk of a neoproliferative response and in-stent restenosis.

Published
2002

Catalog

Books, media, physical & digital resources
See catalog results