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Article ; Online: Response.

Martin, Lukas / Derwall, Matthias / Al Zoubi, Sura / Zechendorf, Elisabeth / Reuter, Daniel A / Thiemermann, Chris / Schuerholz, Tobias

Chest

2019 Volume 156, Issue 3, Page(s) 636–637

Language	English
Publishing date	2019-09-26
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1032552-9
ISSN	1931-3543 ; 0012-3692
ISSN (online)	1931-3543
ISSN	0012-3692
DOI	10.1016/j.chest.2019.05.013
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Article ; Online: Response.

Martin, Lukas / Derwall, Matthias / Al Zoubi, Sura / Zechendorf, Elisabeth / Reuter, Daniel A / Thiemermann, Chris / Schuerholz, Tobias

Chest

2019 Volume 155, Issue 3, Page(s) 647–648

MeSH term(s)	Heart/physiology ; Humans ; Sepsis
Language	English
Publishing date	2019-03-02
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1032552-9
ISSN	1931-3543 ; 0012-3692
ISSN (online)	1931-3543
ISSN	0012-3692
DOI	10.1016/j.chest.2018.10.018
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Article ; Online: Oxygen in the Heart: How Much is too Much?

Kalbitz, Miriam / Waller, Christiane / Huber-Lang, Markus / Gebhard, Florian / Thiemermann, Chris / Radermacher, Peter

Shock (Augusta, Ga.)

2017 Volume 47, Issue 4, Page(s) 531–532

Language	English
Publishing date	2017-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000000760
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Article ; Online: Mesenchymal stromal cells: current understanding and clinical status.

Salem, Husein K / Thiemermann, Chris

Stem cells (Dayton, Ohio)

2009 Volume 28, Issue 3, Page(s) 585–596

Abstract: Multipotent mesenchymal stromal cells (MSCs) represent a rare heterogeneous subset of pluripotent stromal cells that can be isolated from many different adult tissues that exhibit the potential to give rise to cells of diverse lineages. Numerous studies ... ...

Abstract	Multipotent mesenchymal stromal cells (MSCs) represent a rare heterogeneous subset of pluripotent stromal cells that can be isolated from many different adult tissues that exhibit the potential to give rise to cells of diverse lineages. Numerous studies have reported beneficial effects of MSCs in tissue repair and regeneration. After culture expansion and in vivo administration, MSCs home to and engraft to injured tissues and modulate the inflammatory response through synergistic downregulation of proinflammatory cytokines and upregulation of both prosurvival and antiinflammatory factors. In addition, MSCs possess remarkable immunosuppressive properties, suppressing T-cell, NK cell functions, and also modulating dentritic cell activities. Tremendous progress has been made in preclinical studies using MSCs, including the ability to use allogeneic cells, which has driven the application of MSCs toward the clinical setting. This review highlights our current understanding into the biology of MSCs with particular emphasis on the cardiovascular and renal applications, and provides a brief update on the clinical status of MSC-based therapy.
MeSH term(s)	Animals ; Cytokines/immunology ; Cytokines/metabolism ; Humans ; Immune Tolerance/physiology ; Inflammation/immunology ; Leukocytes/immunology ; Mesenchymal Stem Cell Transplantation/methods ; Mesenchymal Stem Cell Transplantation/trends ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/immunology ; Mesenchymal Stem Cells/metabolism ; Stromal Cells/cytology ; Stromal Cells/immunology ; Stromal Cells/metabolism ; Transplantation, Homologous/methods ; Transplantation, Homologous/trends
Chemical Substances	Cytokines
Language	English
Publishing date	2009-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.269
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Article ; Online: The Septic Heart: Current Understanding of Molecular Mechanisms and Clinical Implications.

Martin, Lukas / Derwall, Matthias / Al Zoubi, Sura / Zechendorf, Elisabeth / Reuter, Daniel A / Thiemermann, Chris / Schuerholz, Tobias

Chest

2018 Volume 155, Issue 2, Page(s) 427–437

Abstract: Septic cardiomyopathy is a key feature of sepsis-associated cardiovascular failure. Despite the lack of consistent diagnostic criteria, patients typically exhibit ventricular dilatation, reduced ventricular contractility, and/or both right and left ... ...

Abstract	Septic cardiomyopathy is a key feature of sepsis-associated cardiovascular failure. Despite the lack of consistent diagnostic criteria, patients typically exhibit ventricular dilatation, reduced ventricular contractility, and/or both right and left ventricular dysfunction with a reduced response to volume infusion. Although there is solid evidence that the presence of septic cardiomyopathy is a relevant contributor to organ dysfunction and an important factor in the already complicated therapeutic management of patients with sepsis, there are still several questions to be asked: Which factors/mechanisms cause a cardiac dysfunction associated with sepsis? How do we diagnose septic cardiomyopathy? How do we treat septic cardiomyopathy? How does septic cardiomyopathy influence the long-term outcome of the patient? Each of these questions is interrelated, and the answers require a profound understanding of the underlying pathophysiology that involves a complex mix of systemic factors and molecular, metabolic, and structural changes of the cardiomyocyte. The afterload-related cardiac performance, together with speckle-tracking echocardiography, could provide methods to improve the diagnostic accuracy and guide therapeutic strategies in patients with septic cardiomyopathy. Because there are no specific/causal therapeutics for the treatment of septic cardiomyopathy, the current guidelines for the treatment of septic shock represent the cornerstone of septic cardiomyopathy therapy. This review provides an up-to-date overview of the current understanding of the pathophysiology, summarizes the evidence of currently available diagnostic tools and treatment options, and highlights the importance of further urgently needed studies aimed at improving diagnosis and investigating novel therapeutic targets for septic cardiomyopathy.
MeSH term(s)	Cardiomyopathies/diagnosis ; Cardiomyopathies/etiology ; Cardiomyopathies/physiopathology ; Humans ; Sepsis/complications ; Sepsis/diagnosis ; Sepsis/physiopathology
Language	English
Publishing date	2018-08-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1032552-9
ISSN	1931-3543 ; 0012-3692
ISSN (online)	1931-3543
ISSN	0012-3692
DOI	10.1016/j.chest.2018.08.1037
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Article ; Online: Reduction of the natural Activated protein C pathway activity significantly prevents coagulopathy in a murine model of acute traumatic coagulopathy.

Guerreiro, Maria / Tremoleda, Jordi L / Frith, Dan / Thiemermann, Chris / Brohi, Karim

Scandinavian journal of trauma, resuscitation and emergency medicine

2014 Volume 22, Issue 1, Page(s) 773

Language	English
Publishing date	2014-12
Publishing country	England
Document type	Journal Article
ISSN	1757-7241
ISSN (online)	1757-7241
DOI	10.1186/1757-7241-22-S1-O6
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Article ; Online: Activated Protein C Drives the Hyperfibrinolysis of Acute Traumatic Coagulopathy.

Davenport, Ross A / Guerreiro, Maria / Frith, Daniel / Rourke, Claire / Platton, Sean / Cohen, Mitchell / Pearse, Rupert / Thiemermann, Chris / Brohi, Karim

Anesthesiology

2016 Volume 126, Issue 1, Page(s) 115–127

Abstract: Background: Major trauma is a leading cause of morbidity and mortality worldwide with hemorrhage accounting for 40% of deaths. Acute traumatic coagulopathy exacerbates bleeding, but controversy remains over the degree to which inhibition of procoagulant ...

Abstract	Background: Major trauma is a leading cause of morbidity and mortality worldwide with hemorrhage accounting for 40% of deaths. Acute traumatic coagulopathy exacerbates bleeding, but controversy remains over the degree to which inhibition of procoagulant pathways (anticoagulation), fibrinogen loss, and fibrinolysis drive the pathologic process. Through a combination of experimental study in a murine model of trauma hemorrhage and human observation, the authors' objective was to determine the predominant pathophysiology of acute traumatic coagulopathy. Methods: First, a prospective cohort study of 300 trauma patients admitted to a single level 1 trauma center with blood samples collected on arrival was performed. Second, a murine model of acute traumatic coagulopathy with suppressed protein C activation via genetic mutation of thrombomodulin was used. In both studies, analysis for coagulation screen, activated protein C levels, and rotational thromboelastometry (ROTEM) was performed. Results: In patients with acute traumatic coagulopathy, the authors have demonstrated elevated activated protein C levels with profound fibrinolytic activity and early depletion of fibrinogen. Procoagulant pathways were only minimally inhibited with preservation of capacity to generate thrombin. Compared to factors V and VIII, proteases that do not undergo activated protein C-mediated cleavage were reduced but maintained within normal levels. In transgenic mice with reduced capacity to activate protein C, both fibrinolysis and fibrinogen depletion were significantly attenuated. Other recognized drivers of coagulopathy were associated with less significant perturbations of coagulation. Conclusions: Activated protein C-associated fibrinolysis and fibrinogenolysis, rather than inhibition of procoagulant pathways, predominate in acute traumatic coagulopathy. In combination, these findings suggest a central role for the protein C pathway in acute traumatic coagulopathy and provide new translational opportunities for management of major trauma hemorrhage.
MeSH term(s)	Adult ; Animals ; Blood Coagulation/physiology ; Blood Coagulation Tests/statistics & numerical data ; Cohort Studies ; Disease Models, Animal ; Female ; Fibrinogen/metabolism ; Fibrinolysis/physiology ; Hemorrhage/metabolism ; Hemorrhage/physiopathology ; Humans ; Male ; Mice ; Middle Aged ; Prospective Studies ; Protein C/metabolism ; Thrombelastography ; Wounds and Injuries/blood ; Wounds and Injuries/physiopathology ; Young Adult
Chemical Substances	Protein C ; Fibrinogen (9001-32-5)
Language	English
Publishing date	2016-09-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	269-0
ISSN	1528-1175 ; 0003-3022
ISSN (online)	1528-1175
ISSN	0003-3022
DOI	10.1097/ALN.0000000000001428
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Article: Scavenging Circulating Mitochondrial DNA as a Potential Therapeutic Option for Multiple Organ Dysfunction in Trauma Hemorrhage.

Aswani, Andrew / Manson, Joanna / Itagaki, Kiyoshi / Chiazza, Fausto / Collino, Massimo / Wupeng, Winston Liao / Chan, Tze Khee / Wong, W S Fred / Hauser, Carl J / Thiemermann, Chris / Brohi, Karim

Frontiers in immunology

2018 Volume 9, Page(s) 891

Abstract: Trauma is a leading cause of death worldwide with 5.8 million deaths occurring yearly. Almost 40% of trauma deaths are due to bleeding and occur in the first few hours after injury. Of the remaining severely injured patients up to 25% develop a ... ...

Abstract	Trauma is a leading cause of death worldwide with 5.8 million deaths occurring yearly. Almost 40% of trauma deaths are due to bleeding and occur in the first few hours after injury. Of the remaining severely injured patients up to 25% develop a dysregulated immune response leading to multiple organ dysfunction syndrome (MODS). Despite improvements in trauma care, the morbidity and mortality of this condition remains very high. Massive traumatic injury can overwhelm endogenous homeostatic mechanisms even with prompt treatment. The underlying mechanisms driving MODS are also not fully elucidated. As a result, successful therapies for trauma-related MODS are lacking. Trauma causes tissue damage that releases a large number of endogenous damage-associated molecular patterns (DAMPs). Mitochondrial DAMPs released in trauma, such as mitochondrial DNA (mtDNA), could help to explain part of the immune response in trauma given the structural similarities between mitochondria and bacteria. MtDNA, like bacterial DNA, contains an abundance of highly stimulatory unmethylated CpG DNA motifs that signal through toll-like receptor-9 to produce inflammation. MtDNA has been shown to be highly damaging when injected into healthy animals causing acute organ injury to develop. Elevated circulating levels of mtDNA have been reported in trauma patients but an association with clinically meaningful outcomes has not been established in a large cohort. We aimed to determine whether mtDNA released after clinical trauma hemorrhage is sufficient for the development of MODS. Secondly, we aimed to determine the extent of mtDNA release with varying degrees of tissue injury and hemorrhagic shock in a clinically relevant rodent model. Our final aim was to determine whether neutralizing mtDNA with the nucleic acid scavenging polymer, hexadimethrine bromide (HDMBr), at a clinically relevant time point Conclusions: We have shown that the release of mtDNA is sufficient for the development of multiple organ injury. MtDNA concentrations likely peak at different points in the early postinjury phase dependent on the degree of isolated trauma vs combined trauma and hemorrhagic shock. HDMBr scavenging of circulating mtDNA (and nuclear DNA, nDNA) is associated with rescue from severe multiple organ injury in the animal model. This suggests that HDMBr could have utility in rescue from human trauma-induced MODS.
MeSH term(s)	Adult ; Aged ; Alarmins/immunology ; Alarmins/metabolism ; Animals ; Cohort Studies ; DNA, Bacterial/blood ; DNA, Bacterial/immunology ; DNA, Mitochondrial/blood ; DNA, Mitochondrial/immunology ; Disease Models, Animal ; Female ; Hexadimethrine Bromide/pharmacology ; Hexadimethrine Bromide/therapeutic use ; Humans ; Male ; Middle Aged ; Mitochondria/drug effects ; Mitochondria/immunology ; Mitochondria/metabolism ; Mitochondria/pathology ; Multiple Organ Failure/drug therapy ; Multiple Organ Failure/immunology ; Multiple Organ Failure/mortality ; Multiple Organ Failure/pathology ; Multiple Trauma/drug therapy ; Multiple Trauma/immunology ; Multiple Trauma/mortality ; Multiple Trauma/pathology ; Prospective Studies ; Rats, Wistar ; Shock, Hemorrhagic/drug therapy ; Shock, Hemorrhagic/immunology ; Shock, Hemorrhagic/mortality ; Shock, Hemorrhagic/pathology ; Trauma Severity Indices ; Treatment Outcome ; Young Adult
Chemical Substances	Alarmins ; DNA, Bacterial ; DNA, Mitochondrial ; Hexadimethrine Bromide (4C905MSK4W)
Language	English
Publishing date	2018-05-08
Publishing country	Switzerland
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.00891
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Article ; Online: Inhibition of glycogen synthase kinase (GSK)-3-β improves liver microcirculation and hepatocellular function after hemorrhagic shock.

Jellestad, Lena / Fink, Tobias / Pradarutti, Sascha / Kubulus, Darius / Wolf, Beate / Bauer, Inge / Thiemermann, Chris / Rensing, Hauke

European journal of pharmacology

2014 Volume 724, Page(s) 175–184

Abstract: Ischemia and reperfusion may cause liver injury and are characterized by hepatic microperfusion failure and a decreased hepatocellular function. Inhibition of glycogen synthase kinase (GSK)-3β, a serine-threonine kinase that has recently emerged as a key ...

Abstract	Ischemia and reperfusion may cause liver injury and are characterized by hepatic microperfusion failure and a decreased hepatocellular function. Inhibition of glycogen synthase kinase (GSK)-3β, a serine-threonine kinase that has recently emerged as a key regulator in the modulation of the inflammatory response after stress events, may be protective in conditions like sepsis, inflammation and shock. Therefore, aim of the study was to assess the role of GSK-3β in liver microcirculation and hepatocellular function after hemorrhagic shock and resuscitation (H/R). Anesthetized male Sprague-Dawley rats underwent pretreatment with Ringer´s solution, vehicle (DMSO) or TDZD-8 (1 mg/kg), a selective GSK-3β inhibitor, 30 min before induction of hemorrhagic shock (mean arterial pressure 35±5 mmHg for 90 min) and were resuscitated with shed blood and Ringer´s solution (2h). 5h after resuscitation hepatic microcirculation was assessed by intravital microscopy. Propidium iodide (PI) positive cells, liver enzymes and alpha-GST were measured as indicators of hepatic injury. Liver function was estimated by assessment of indocyanine green plasma disappearance rate. H/R led to a significant decrease in sinusoidal diameters and impairment of liver function compared to sham operation. Furthermore, the number of PI positive cells in the liver as well as serum activities of liver enzymes and alpha-GST increased significantly after H/R. Pretreatment with TDZD-8 prevented the changes in liver microcirculation, hepatocellular injury and liver function after H/R. A significant rise in the plasma level of IL-10 was observed. Thus, inhibition of GSK-3β before hemorrhagic shock modulates the inflammatory response and improves hepatic microcirculation and hepatocellular function.
MeSH term(s)	Alanine Transaminase/blood ; Animals ; Aspartate Aminotransferases/blood ; Glutamate Dehydrogenase/blood ; Glutathione Transferase/blood ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/metabolism ; Glycogen Synthase Kinase 3 beta ; Hepatocytes/drug effects ; Hepatocytes/pathology ; Interleukin-10/blood ; Liver/blood supply ; Liver/drug effects ; Male ; Microcirculation/drug effects ; Rats ; Rats, Sprague-Dawley ; Regional Blood Flow/drug effects ; Shock, Hemorrhagic/blood ; Shock, Hemorrhagic/physiopathology ; Thiadiazoles/pharmacology ; Tumor Necrosis Factor-alpha/blood
Chemical Substances	4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione ; Thiadiazoles ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; Glutamate Dehydrogenase (EC 1.4.1.2) ; Glutathione Transferase (EC 2.5.1.18) ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Gsk3b protein, rat (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2014-02-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2013.12.029
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Article ; Online: Chemical and biochemical characterization and in vivo safety evaluation of pharmaceuticals in drinking water.

de Jesus Gaffney, Vanessa / Mota-Filipe, Helder / Pinto, Rui Amaro / Thiemermann, Chris / Loureiro, Marta / Cardoso, Vitor Vale / Benoliel, Maria João / Almeida, Cristina M M

Environmental toxicology and chemistry

2016 Volume 35, Issue 11, Page(s) 2674–2682

Abstract: The water constituents that are currently subject to legal control are only a small fraction of the vast number of chemical substances and microorganisms that may occur in both the environment and water resources. The main objective of the present study ... ...

Abstract	The water constituents that are currently subject to legal control are only a small fraction of the vast number of chemical substances and microorganisms that may occur in both the environment and water resources. The main objective of the present study was to study the health impact resulting from exposure to a mixture of pharmaceuticals that have been detected in tap water at low doses. Analyses of atenolol, caffeine, erythromycin, carbamazepine, and their metabolites in blood, urine, feces, fat tissue, liver, and kidney after exposure to a mixture of these pharmaceuticals in treated drinking water were performed. The effects of this exposure were assessed in rats by measuring biochemical markers of organ injury or dysfunction. Simultaneously, the selected pharmaceuticals were also quantified in both physiological fluids and organ homogenates by liquid chromatography-tandem mass spectrometry (performed in multiple reaction monitoring mode and full scan mode). Following exposure of rats to a concentration of a pharmaceutical which was 10 times higher than the concentration known to be present in tap water, trace levels of some pharmaceuticals and their metabolites were detected in biological samples. This exposure did, however, not lead to significant organ injury or dysfunction. Thus, the authors report an experimental model that can be used to characterize the safety profile of pharmaceuticals in treated drinking water using a multiorgan toxicity approach. Environ Toxicol Chem 2016;35:2674-2682. © 2016 SETAC.
MeSH term(s)	Animals ; Caffeine/analysis ; Caffeine/urine ; Carbamazepine/analysis ; Carbamazepine/urine ; Chromatography, High Pressure Liquid ; Drinking Water/chemistry ; Environmental Exposure ; Erythromycin/analysis ; Erythromycin/urine ; Kidney/metabolism ; Liver/metabolism ; Models, Theoretical ; Pharmaceutical Preparations/analysis ; Pharmaceutical Preparations/urine ; Rats ; Rats, Wistar ; Tandem Mass Spectrometry ; Water Purification/methods
Chemical Substances	Drinking Water ; Pharmaceutical Preparations ; Carbamazepine (33CM23913M) ; Caffeine (3G6A5W338E) ; Erythromycin (63937KV33D)
Language	English
Publishing date	2016-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	46234-2
ISSN	1552-8618 ; 0730-7268
ISSN (online)	1552-8618
ISSN	0730-7268
DOI	10.1002/etc.3451
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