Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Tobias J. Krämer"'
Autor:
Ralph Timaru-Kast, Shila P. Coronel-Castello, Tobias J. Krämer, André V. Hugonnet, Michael K. E. Schäfer, Anne Sebastiani, Serge C. Thal
Publikováno v:
Scientific Reports, Vol 13, Iss 1, Pp 1-20 (2023)
Abstract After traumatic brain injury (TBI) cerebral inflammation with invasion of neutrophils and lymphocytes is a crucial factor in the process of secondary brain damage. In TBI the intrinsic renin-angiotensin system is an important mediator of cer
Externí odkaz:
https://doaj.org/article/2557f8d681d34b98b46b06fc3d1b1c2e
Autor:
Tobias J. Krämer, Florian Pickart, Bruno Pöttker, Christina Gölz, Axel Neulen, Tobias Pantel, Hermann Goetz, Katharina Ritter, Michael K. E. Schäfer, Serge C. Thal
Publikováno v:
Scientific Reports, Vol 13, Iss 1, Pp 1-12 (2023)
Abstract Traumatic brain injury (TBI) causes the release of danger-associated molecular patterns (DAMP) from damaged or dead cells, which contribute to secondary brain damage after TBI. Cell-free DNA (cfDNA) is a DAMP known to cause disruption of the
Externí odkaz:
https://doaj.org/article/86feabec15364ca8b03bfda43c74c694
Autor:
Ralph Timaru-Kast, Andreas Garcia Bardon, Clara Luh, Shila P. Coronel-Castello, Phuriphong Songarj, Eva-Verena Griemert, Tobias J. Krämer, Anne Sebastiani, Ulrike Muscha Steckelings, Serge C. Thal
Publikováno v:
Scientific Reports, Vol 12, Iss 1, Pp 1-13 (2022)
Abstract Antagonism of the angiotensin II type 1 receptor (AT1) improves neurological function and reduces brain damage after experimental traumatic brain injury (TBI), which may be partly a result of enhanced indirect angiotensin II type 2 receptor
Externí odkaz:
https://doaj.org/article/e329d91b9d42476d86ee249c7dc88eb5
Autor:
Tobias J. Krämer, Per Hübener, Bruno Pöttker, Christina Gölz, Axel Neulen, Tobias Pantel, Hermann Goetz, Katharina Ritter, Michael K. E. Schäfer, Serge C. Thal
Publikováno v:
Scientific Reports, Vol 12, Iss 1, Pp 1-10 (2022)
Abstract Traumatic brain injury (TBI) involves primary mechanical damage and delayed secondary damage caused by vascular dysfunction and neuroinflammation. Intracellular components released into the parenchyma and systemic circulation, termed danger-
Externí odkaz:
https://doaj.org/article/0ce2da96cf5846cca14e90f9009e0a54
Autor:
Tobias J. Krämer, Nathalia Hack, Till J. Brühl, Lutz Menzel, Regina Hummel, Eva-Verena Griemert, Matthias Klein, Serge C. Thal, Tobias Bopp, Michael K. E. Schäfer
Publikováno v:
Journal of Neuroinflammation, Vol 16, Iss 1, Pp 1-14 (2019)
Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate t
Externí odkaz:
https://doaj.org/article/53c8f9ff3c2a4a2aaf5e47b6442e117e
Autor:
Tobias J. Krämer, Wasim Sakas, Daniel Jussen, Harald Krenzlin, Oliver Kempski, Beat Alessandri
Publikováno v:
BMC Neuroscience, Vol 19, Iss 1, Pp 1-12 (2018)
Abstract Background Acute subdural hemorrhage (ASDH) is a severe consequence of traumatic brain injury. The occurrence of subdural blood increases the lethality of these patients independent of the amount of blood or elevated intracranial pressure. T
Externí odkaz:
https://doaj.org/article/83423834e659417b8e3b4947c267c655
Autor:
Tobias J. Krämer, Nathalia Hack, Till J. Brühl, Lutz Menzel, Regina Hummel, Eva-Verena Griemert, Matthias Klein, Serge C. Thal, Tobias Bopp, Michael K. E. Schäfer
Publikováno v:
Journal of Neuroinflammation, Vol 16, Iss 1, Pp 1-1 (2019)
Following publication of the original article [1], the authors opted to correct the following mistakes. According to the title and our results, the conclusions in the abstract and at the end of the discussion the term “attenuates” must be correct
Externí odkaz:
https://doaj.org/article/2075accaa5364a5a8850f652380a8e5f
Autor:
Ralph Timaru-Kast, Shila P. Coronel-Castello, Tobias J. Krämer, André V. Hugonnet, Michael K. E. Schäfer, Anne Sebastiani, Serge C. Thal
Cerebral inflammation with invasion of neutrophils and lymphocytes is a crucial factor in the process of secondary brain damage after traumatic brain injury (TBI). In TBI the intrinsic renin-angiotensin system is an important mediator of cerebral inf
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ceb9b825a85b6957afa63c6e246da3ce
https://doi.org/10.21203/rs.3.rs-2110098/v1
https://doi.org/10.21203/rs.3.rs-2110098/v1
Autor:
Tobias J. Krämer, Per Hübener, Bruno Pöttker, Christina Gölz, Axel Neulen, Tobias Pantel, Hermann Goetz, Katharina Ritter, Serge C Thal, Michael K.E. Schäfer
Traumatic brain injury (TBI) involves primary mechanical damage and delayed secondary damage caused by vascular dysfunction and neuroinflammation. Intracellular components released into the parenchyma and systemic circulation, termed danger-associate
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::67d9ac07b0b9290472232f163979c54b
https://doi.org/10.21203/rs.3.rs-956514/v1
https://doi.org/10.21203/rs.3.rs-956514/v1