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2. Correction to: Phenytoin inhibits necroptosis

Author

von Mässenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stéphane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, Anders, Hans Joachim, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, and Linkermann, Andreas

Published
2018
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3. Phenytoin inhibits necroptosis

Author

von Mässenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stéphane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, Anders, Hans Joachim, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, and Linkermann, Andreas

Published
2018
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6. Optimized procedures for diagnostic testing for pheochromocytoma and paraganglioma in patients on hemodialysis

Author

Pamporaki, Christina, primary, Prejbisz, Aleksander, additional, Małecki, Robert, additional, Pistrosch, Frank, additional, Peitzsch, Mirko, additional, Bishoff, Steffen, additional, Mueller, Petra, additional, Meyer, Iris, additional, Reimann, Doreen, additional, Hanus, Katarzyna, additional, Januszewicz, Andrzej, additional, Bornstein, Stefan, additional, Parmentier, Simon, additional, Kunath, Carola, additional, Lenders, Jacques, additional, Eisenhofer, Graeme, additional, and Passauer, Jens, additional

Published
2021
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9. Comparative study of microvascular function: Forearm blood flow versus dynamic retinal vessel analysis.

Author

Schirutschke, Holger, Kochan, Johannes, Haink, Kristin, Rettig, Ronny, Parmentier, Simon Paul, Ziemssen, Tjalf, and Passauer, Jens

Subjects
BLOOD flow, RETINAL blood vessels, FOREARM, BRACHIAL artery, UNITS of measurement
Abstract

Objective: Recently, dynamic retinal vessel analysis (DVA) has gained interest for investigation of microvascular function but comparative measurements with standard methods like the forearm blood flow technique (FBF) are uncommon till now. Methods: We recruited 23 high‐risk cardiovascular patients (Risk) and 17 healthy persons (Ctrl). During the FBF experiment, postocclusive reactive hyperaemia (RH) as well as endothelium‐dependent and independent vasodilation was measured by infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) into the brachial artery. The dynamic vessel analyzer was applied for measurement of the retinal arterial and venous response to flickering light during DVA and for determination of the central retinal arterial (CRAE) and venous equivalent (CRVE). Results: Forearm blood flow technique was significantly attenuated in the patient group during postocclusive RH (p <.005). The increase of FBF in response to SNP did not differ significantly between the two groups (p =.09). In contrast, the FBF response to ACh was significantly blunted in the patient group (p <.05), indicating endothelial dysfunction. DVA did not detect any difference of retinal arterial (p =.68) or retinal venous (p =.93) vasodilation between both groups. The CRAE (p =.55) and CRVE (p =.83) did not differ significantly in either group. Conclusions: Forearm blood flow and DVA cannot be regarded as equivalent methods for testing of microvascular function. Possible explanations include differences in the vascular beds and vessel diameters examined as well as differences in the trigger mechanisms applied. Further studies are needed to define the role of DVA in this context. [ABSTRACT FROM AUTHOR]

Published
2021
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11. We AIM2 Inflame

Author

Linkermann, Andreas, primary, Parmentier, Simon P., additional, and Hugo, Christian, additional

Published
2018
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12. Phenytoin inhibits necroptosis

Author

von Maessenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stephane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, Anders, Hans Joachim, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, Linkermann, Andreas, von Maessenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stephane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, Anders, Hans Joachim, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, and Linkermann, Andreas

Abstract

Receptor-interacting protein kinases 1 and 3 (RIPK1/3) have best been described for their role in mediating a regulated form of necrosis, referred to as necroptosis. During this process, RIPK3 phosphorylates mixed lineage kinase domain like (MLKL) to cause plasma membrane rupture. RIPK3-deficient mice have recently been demonstrated to be protected in a series of disease models, but direct evidence for activation of necroptosis in vivo is still limited. Here, we sought to further examine the activation of necroptosis in kidney ischemia-reperfusion injury (IRI) and from TNF alpha-induced severe inflammatory response syndrome (SIRS), two models of RIPK3-dependent injury. In both models, MLKL-ko mice were significantly protected from injury to a degree that was slightly, but statistically significantly exceeding that of RIPK3-deficient mice. We also demonstrated, for the first time, accumulation of pMLKL in the necrotic tubules of human patients with acute kidney injury. However, our data also uncovered unexpected elevation of blood flow in MLKL-ko animals, which may be relevant to IRI and should be considered in the future. To further understand the mode of regulation of cell death by MLKL, we screened a panel of clinical plasma membrane channel blockers and we found phenytoin to inhibit necroptosis. However, we further found that phenytoin attenuated RIPK1 kinase activity in vitro, likely due to the hydantoin scaffold also present in necrostatin-1, and blocked upstream necrosome formation steps in the cells undergoing necroptosis. We further report that this clinically used anticonvulsant drug displayed protection from kidney IRI and TNF alpha-induces SIRS in vivo. Overall, our data reveal the relevance of RIPK3-pMLKL regulation for acute kidney injury and identifies an FDA-approved drug that may be useful for immediate clinical evaluation of inhibition of pro-death RIPK1/RIPK3 activities in human diseases.

Published
2018

13. Phenytoin inhibits necroptosis (vol 9, 359, 2018)

Author

von Maessenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stephane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, JoachimAnders, Hans, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, Linkermann, Andreas, von Maessenhausen, Anne, Tonnus, Wulf, Himmerkus, Nina, Parmentier, Simon, Saleh, Danish, Rodriguez, Diego, Ousingsawat, Jiraporn, Ang, Rosalind L., Weinberg, Joel M., Sanz, Ana B., Ortiz, Alberto, Zierleyn, Adrian, Becker, Jan Ulrich, Baratte, Blandine, Desban, Nathalie, Bach, Stephane, Schiessl, Ina Maria, Nogusa, Shoko, Balachandran, Siddharth, JoachimAnders, Hans, Ting, Adrian T., Bleich, Markus, Degterev, Alexei, Kunzelmann, Karl, Bornstein, Stefan R., Green, Douglas R., Hugo, Christian, and Linkermann, Andreas

Published
2018

16. The clinical relevance of necroinflammation—highlighting the importance of acute kidney injury and the adrenal glands

Author

Tonnus, Wulf, Gembardt, Florian, Latk, Markus, Parmentier, Simon, Hugo, Christian, Bornstein, Stefan R., and Linkermann, Andreas

Abstract

Necroinflammation is defined as the inflammatory response to necrotic cell death. Different necrotic cell death pathways exhibit different immune reponses, despite a comparable level of intracellular content release (referred to as damage associated molecular patterns or DAMPs). In addition to DAMP release, which is inevitably associated with necrotic cell death, the active production of pro/anti-inflammatory cytokines characterizes certain necrotic pathways. Necroptosis, ferroptosis and pyroptosis, therefore, are immunogenic to a different extent. In this review, we discuss the clinical relevance of necroinflammation highlighting potential human serum markers. We focus on the role of the adrenal glands and the lungs as central organs affected by systemic and/or local DAMP release and underline their role in intensive care medicine. In addition, data from models of acute kidney injury (AKI) and kidney transplantation have significantly shaped the field of necroinflammation and may be helpful for the understanding of the potential role of dialysis and plasma exchange to treat ongoing necroinflammation upon intensive care unit (ICU) conditions. In conclusion, we are only beginning to understand the importance of necroinflammation in diseases and transplantation, including xenotransplantation. However, given the existing efforts to develop inhibitors of necrotic cell death (ferrostatins, necrostatins, etc), we consider it likely that interference with necroinflammation reaches clinical routine in the near future.

Published
2019
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19. Peritoneal dialysis - 2

Author

Yosshimi Sekiguchi, Sydney S.C. Tang, Ka Ying Tam, Pieter Ter Wee, Masato Kasahara, Takuma Hazama, Muhammad Shahed Ahmed, Luis Michea, Martina Pechula Thut, Begoña Rivas, Sang Choel Lee, Ana Salazar, Stephen G. John, Steven McTaggart, Isabel Martín, Takashige Kuwabara, Jens Schewe, Miguel Angel Suárez, Fu-Chang Hu, Jose A. Sanchez-Tomero, Valeria Aicardi, Iris Rafalia, Władysław Sułowicz, Giancarlo Lavoratti, Naoto Miura, Rigas Kalaitzidis, Parmentier Simon, Carolyn Clark, Eve Chowaniec, Vitor Ramalho, Guadalupe Gonzalez, Haiping Mao, Ilse Maria Ratsch, Yi-Sheng Lin, Dan-Xia Zheng, Qing-Feng Han, Amit Gupta, Michał Chmielewski, Marcin Renke, Catrin Palm, Kwan-Dun Wu, Katarzyna Janda, Chieko Hamada, Richard Baer, Mooyong Park, Stephan Segerer, Miguel Perez Fontan, Seongah Hong, Natalia Blanco Castro, Marcin Krzanowski, Masashi Mukoyama, Hossam El-Shazly, J.E. Sanchez, Anneleen Pletinck, Da-Hong Wang, Carmen Cámara, Carmel M. Hawley, Franziska Belling, Przemysław Miarka, Rudolf P. Wuethrich, Shvan Korsheed, Mohammed Al-Azmi, Roberto Chimenz, Tao Wang, Konstantinos Siamopoulos, Marcel Schouten, Zhikai Yang, Tetsutaro Shimaoka, Elisabeth W. Boeschoten, Rubén Torres, Beata Kusnierz, Yasuhiko Ito, Walter Douthat, Matthias Sauter, Hameed Anijeet, Vivian Fathi, Beatriz Malvar, Margarita Economou, Yukihiro Kimura, Yoko Hotta, Bruno Gianoglio, Alan Cass, Angelines Domínguez, Inés Castellano, Teresa Bellón, M. Auxiliadora Bajo, Tomohito Matsunaga, Sandra Gallego, Enrico Vidal, Jenq-Wen Huang, Antonio Fernandez-Perpen, Manuel Amoedo, Esteban Romero, Tun-Jun Tsai, Manoel Pacheco Andrade, Yusuke Kaida, Keiichi Takiue, Karolina Kotewicz, Hisako Muramatsu, Paraskevi Tseke, Hiroaki Io, P. Vidau, Liliana Gomez, Helen Jefferies, Agostinho S. Carvalho, Kiyoshi Mori, Juan Ramón Gómez-Martino, Gert A. Verpooten, Alicia Smith, Richard Fluck, Jonas Axelsson, Giovanna Leozappa, Seung-Duk Hwang, Bolesław Rutkowski, Paul Snelling, Hiroshi Morinaga, Xiao Yang, Yung-Ming Chen, Gloria del Peso, Clara Molina, M. Joao Carvalho, Sara Estupiñan, Tak Mao Chan, Wai-Kei Lo, Jing Nie, Carmine Pecoraro, Seung Hyeok Han, Ea Wha Kang, Konstantinos Katopodis, Alberto Edefonti, David W. Johnson, Magdalena Gonzalez, Bartosz Skonieczny, Soo-Jeong Choi, Tomoko Kawanishi, George Spanos, M Jose Castro, Rafael Selgas, T. Ortega, Markus Wörnle, Inna Kolesnyk, Geoffrey Playford, Ching-Hsiu Peng, Tomasz Liberek, Rie Kitamura, Kay Herbrig, Jie Dong, Natasha J. McIntyre, C. Rodriguez, Li-Tao Cheng, Hugo Poblete, Auxiliadora Bajo, Hideki Yokoi, Jutta Passlick-Deetjen, M. Luisa Perez-Lozano, Ayako Fujimi, Yohei Maeshima, Liqiong Hu, Daijiro Masamoto, Raj Kumar Sharma, Manuel Lopez-Cabrera, Antonio Cabrita, Wim Van Biesen, Frans J. van Ittersum, Andres Stutzin, Javier de Arteaga, Y.Z. Shah, Wim Rüger, Hideharu Tanaka, Christopher W. McIntyre, Archna Sinha, Ai-Hua Zhang, Baltasar Lucendo, Thomas Sitter, Nari Kim, Anita Saxena, Amaia Ros, Shili Zhao, Ryuji Iwatani, Kei Fukami, Miriam Alvo, Seiichi Matsuo, Takahiro Kuragano, Yuko Inami, James O. Burton, Tang Li, Karin Janssen van Doorn, Luiz Comazzetto, M. Martin, Qiongqiong Yang, Masayoshi Nanami, Man-Lai Chu, Sho-ichi Yamagishi, Yoshimi Takamiya, Angela Bento, Roland Ladurner, Man Fei Lam, Silvio Maringhini, Takeshi Nakanishi, Pablo U. Massari, Szu-Chun Hung, Eleni Triantou, C. Garcia-Cueto, John Paul Killen, Kate Kendall, Enrico Verrina, Filipa Vilhena, Yukiko Hasuike, Olga Balafa, Julio Bittar, Jiro Inuma, Y. Ogawa, Li Zuo, Jorge L. De La Fuente, Mariane B.R. Martins, Wanbok Lee, Aritoshi Kida, Adriana Coutinho, Raymond T. Krediet, Rafael Sánchez-Villanueva, Yaning Wang, Jacek Kot, Jin Kuk Kim, Hiroshi Nonoguchi, Bassam Al-Helal, João Aniceto, Amal Hassan, Kazuwa Nakao, Fabian Ledesma, Seiji Ueda, M. Joao Rocha, Fernanda L. Lima, Jose Cabeda, Thomas Mussack, Nora Gad, Stephane Heritier, Eduardo Lorca, Seiya Okuda, Hirotaka Imamaki, Man-Fai Lam, Ana Luisa Eguiguren, Kar-Neng Lai, Luciana M.M. Barbosa, Yasuhiko Tomino, Andres Lopez Muñiz, João Victor Duarte Lobo, Joseph Leung, Lindsay J. Chesterton, Maria Van Landschoot, Virginia Martínez, Dae Suk Han, Midoriko Watanabe, Bengt Lindholm, Yoko Saito, Jolanta Kowalewska, Hon-Yen Wu, Friedo W. Dekker, Hitoshi Sugiyama, Jens Passauer, Elaine Beller, Anabela S. Rodrigues, Kar Neng Lai, Ricardo Santos, Anupama Kaul, Naser Hussain, Ximena Rocca, Alejandro Pacheco, Carlos Chiurchiu, Zhewen Zhong, Akira Sugawara, Raymond Vanholder, Helena Diaz Cambre, Vlado Perkovic, Hayato Nishimura, Tatsuyuki Inoue, Hirofumi Makino, Luisa Murer, Narayan Prasad, Anabela Malho, Janak de Zoysa, Ali Attaia, Charles Thompson, Masuo Obinata, Andrea Ribeiro, Katsukiyo Ito, Takuo Kusumoto, Kiyomi Koike, Monika Lichodziejewska-Niemierko, Keiki Ogino, Wei Chen, Kuan-Yu Hung, Norihiro Suga, Jinjin Fan, Nicole N. Isbel, Xueqing Yu, E. Gago, Der-Cherng Tarng, Ana Rodriguez-Carmona, Tomasz Stompór, Shinji Kitamura, Isabel Fonseca, Nabieh Al-Hilali, Takashi Muramatsu, Murty Mantha, Pedro Pessegueiro, Kleyton A. Bastos, Yoshinaga Otaki, Marc Van den Bossche, Sanne E. Hoeks, Mi-Suen Lee, Noriyoshi Masuoka, Qunying Guo, Ruixi Li, Alf Corsenca, Macarena Arancibia, Seiki Aruga, Luiz S. Aroeira, Carlos Pires, B. Diaz-Molina, Kayo Kaneko, Hirokazu Imai, Palma Sorino, Shigeru Akagi, Paul Owen, Ko-Lin Kuo, Fengxin Zhu, Teresa Garcia Falcon, Xueqin Wang, Takuya Seto, and Ana Marta Gomes

Subjects
Transplantation, medicine.medical_specialty, Nephrology, business.industry, medicine.medical_treatment, medicine, Urology, business, Peritoneal dialysis
Published
2009
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20. Injured kidney endothelium is only marginally repopulated by cells of extrarenal origin.

Author

Schirutschke, Holger, Vogelbacher, Regina, Stief, Andrea, Parmentier, Simon, Daniel, Christoph, and Hugo, Christian

Subjects
BONE marrow diseases, KIDNEY abnormalities, NEPHRECTOMY, ENDOTHELIAL cells, CHIMERISM, ENDOTHELIUM physiology
Abstract

The role of bone marrow marrow-derived cells after kidney endothelial injury is controversial. In this study, we investigated if and to what extent extrarenal cells incorporate into kidney endothelium after acute as well as during chronic endothelial injury. Fischer F-344wt (wild type) rat kidney grafts were transplanted into R26-hPAP (human placental alkaline phosphatase) transgenic Fischer F-344 recipient rats to allow identification of extrarenal cells by specific antibody staining. A severe model of renal thrombotic microangiopathy was induced via graft perfusion with antiglomerular endothelial cell (GEN) antibody and resulted in eradication of 85% of the glomerular and 69% of the peritubular endothelium (GEN group). At week 4 after injury, renal endothelial healing as well as recovery of the kidney function was seen. Endothelial chimerism was evaluated by double staining for hPAP and endothelial markers RECA-1 or JG-12. Just 0.25% of the glomerular and 0.1% of the peritubular endothelium was recipient derived. In a second experiment, chronic endothelial injury was induced by combination of kidney transplantation with 5/6 nephrectomy (5/6 Nx group). After 14 wk, only 0.86% of the peritubular and 0.05% of the glomerular endothelium was of recipient origin. In summary, despite demonstration of extensive damage and loss as well as excellent regeneration, just a minority of extrarenal cells were incorporated into kidney endothelium in rat models of acute and chronic renal endothelial cell injury. Our results highlight that kidney endothelial regeneration after specific and severe injury is almost exclusively of renal origin. [ABSTRACT FROM AUTHOR]

Published
2013
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21. Extrarenal Progenitor Cells Do Not Contribute to Renal Endothelial Repair.

Author

Sradnick J, Rong S, Luedemann A, Parmentier SP, Bartaun C, Todorov VT, Gueler F, Hugo CP, and Hohenstein B

Subjects
Animals, Bone Marrow Cells, Endothelium physiology, Mice, Mice, Inbred C57BL, Endothelial Cells physiology, Kidney cytology, Stem Cells physiology
Abstract

Endothelial progenitor cells (EPCs) may be relevant contributors to endothelial cell (EC) repair in various organ systems. In this study, we investigated the potential role of EPCs in renal EC repair. We analyzed the major EPC subtypes in murine kidneys, blood, and spleens after induction of selective EC injury using the concanavalin A/anti-concanavalin A model and after ischemia/reperfusion (I/R) injury as well as the potential of extrarenal cells to substitute for injured local EC. Bone marrow transplantation (BMTx), kidney transplantation, or a combination of both were performed before EC injury to allow distinction of extrarenal or BM-derived cells from intrinsic renal cells. During endothelial regeneration, cells expressing markers of endothelial colony-forming cells (ECFCs) were the most abundant EPC subtype in kidneys, but were not detected in blood or spleen. Few cells expressing markers of EC colony-forming units (EC-CFUs) were detected. In BM chimeric mice (C57BL/6 with tandem dimer Tomato-positive [tdT+] BM cells), circulating and splenic EC-CFUs were BM-derived (tdT+), whereas cells positive for ECFC markers in kidneys were not. Indeed, most BM-derived tdT+ cells in injured kidneys were inflammatory cells. Kidneys from C57BL/6 donors transplanted into tdT+ recipients with or without prior BMTx from C57BL/6 mice were negative for BM-derived or extrarenal ECFCs. Overall, extrarenal cells did not substitute for any intrinsic ECs. These results demonstrate that endothelial repair in mouse kidneys with acute endothelial lesions depends exclusively on local mechanisms., (Copyright © 2016 by the American Society of Nephrology.)

Published
2016
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