Thomas Bertsch

Publications (55)168.53 Total impact

• Article: Evaluation of the automated coagulation analyzer Sysmex CA-7000.

  Alexandra Dorn-Beineke, Carl-Erik Dempfle, Thomas Bertsch, Herrmann Wisser
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  ABSTRACT: Centralization of laboratory diagnostics and an increasing number of urgent requests and nonstandard samples raise the need for short turn-around times and high-throughput analyzers for coagulation tests. The aim of the present study was to evaluate the analytical and technical performance of the Sysmex CA-7000 coagulation analyzer under routine laboratory conditions. We evaluated the Sysmex CA-7000 in comparison to the Sysmex CA-6000 analyzer for PT, INR, aPTT, Clauss, and derived fibrinogen. We also compared antithrombin (AT) measured on the Sysmex CA-7000 and Dimension RxL. Imprecision studies were performed, and throughput, online, and STAT functions and the handling of routine samples were evaluated. The Sysmex CA-7000 showed very low intra-assay and interassay variability for all parameters. The method comparison study showed good comparability to the Sysmex CA-6000 and Dimension RxL. The throughput of the Sysmex CA-7000 was 2.5--3 times faster than that of Sysmex CA-6000. No interference was seen for total bilirubin up to 710 micromol/L. Triglyceride levels >11.4 mmol/L resulted in invalid PT measurements and levels >3.42 mmol/L gave invalid results for Clauss fibrinogen on the CA-7000 analyzer. This is the first published evaluation of the analytical and technical performance of the coagulation analyzer Sysmex CA-7000. We conclude that the CA-7000 is well suited for coagulation laboratories with high sample throughput and a high number of nonstandard samples.
  Thrombosis Research 01/2005; 116(2):171-9. · 2.44 Impact Factor
• Article: High doses of simvastatin, pravastatin, and cholesterol reduce brain cholesterol synthesis in guinea pigs.

  Dieter Lütjohann, Mark Stroick, Thomas Bertsch, Sandra Kühl, Bernhard Lindenthal, Karin Thelen, Ulla Andersson, Ingemar Björkhem, Klaus von Bergmann Kv, Klaus Fassbender
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  ABSTRACT: Recent epidemiological studies suggest that inhibitors of 3-hydroxy-3-methyl-glutaryl CoA reductase, so-called statins, are effective in lowering the prevalence of Alzheimer's disease. Whether the effect of statins is due to a local inhibition of cholesterol synthesis in the brain or whether it is mediated by the reduced levels of cholesterol in the circulation is not known. In the present work, we tested the possibility that high doses of lipophilic and hydrophilic statins, simvastatin and pravastatin, respectively, or a diet high in cholesterol could affect cholesterol homeostasis in the brain of guinea pigs. The total brain cholesterol levels were not affected by high-dose simvastatin or pravastatin treatment. Significantly lower levels of the cholesterol precursor lathosterol and its ratio to cholesterol were found in the brains of simvastatin and pravastatin-treated animals. 24S-Hydroxycholesterol, the transportable form of cholesterol across the blood-brain barrier, was significantly lower in the brain of pravastatin-treated animals. Excessive cholesterol feeding resulted in higher serum cholesterol levels but did not affect total brain cholesterol level. However, de novo cholesterol synthesis in the brain seemed to be down-regulated, as indicated by lower absolute levels and cholesterol-related ratios of lathosterol compared with controls. The passage of deuterium-labeled cholesterol across the blood-brain barrier in one animal was found to be approximately 1%. Our results suggest that brain cholesterol synthesis in guinea pigs can be slightly, but significantly, influenced by high doses of lipophilic and hydrophilic statins as well as by high dietary cholesterol intake, while total brain cholesterol content and thus, cholesterol homeostasis is maintained.
  Steroids 07/2004; 69(6):431-8. · 2.83 Impact Factor
• Article: Markers of myocardial damage, tissue healing, and inflammation after radiofrequency catheter ablation of atrial tachyarrhythmias.

  Martina Brueckmann, Christian Wolpert, Thomas Bertsch, Tim Sueselbeck, Claudia Liebetrau, Jens J Kaden, Guenter Huhle, Michael Neumaier, Martin Borggrefe, Karl K Haase
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  ABSTRACT: Radiofrequency ablation produces a localized endomyocardial necrosis that may result in release of biochemical markers reflecting myocardial cell damage, inflammation, and tissue reparation. The aim of this study was to determine the extent of rise and time course of markers of inflammation and tissue reparation in patients undergoing radiofrequency catheter ablation. Serial blood samples were taken from patients with AV nodal reentrant tachycardia (n = 5), Wolff-Parkinson-White syndrome (n = 3), and atrial flutter (n = 5) undergoing radiofrequency ablation. Blood was taken before ablation (day 0, baseline) and at day 1 and day 120 after ablation. The proinflammatory marker interleukin-6 (IL-6), troponin I (TNI), and myoglobin, as well as matrix metalloproteinase-9 (MMP-9), a marker for myocardial healing, were measured by enzyme-linked immunosorbent assay. Levels of IL-6, TNI, myoglobin, and MMP-9 were significantly elevated on day 1 after ablation compared to baseline levels. Seven of the 13 patients had troponin levels greater than the threshold of significant myocardial damage (>0.1 ng/mL) on day 1. Plasma levels of MMP-9 were still elevated on day 120 compared to values before ablation (P = 0.021). Markers of inflammation, wound healing, and myocardial damage are increased in patients who undergo radiofrequency ablation. Levels of MMP-9, a marker for myocardial healing and repair, are still elevated 120 days after the procedure, suggesting that radiofrequency ablation induces tissue damage leading to a long-term process of reparation.
  Journal of Cardiovascular Electrophysiology 06/2004; 15(6):686-91. · 3.06 Impact Factor
• Article: Time course of systemic markers of inflammation in patients presenting with acute coronary syndromes.

  Martina Brueckmann, Thomas Bertsch, Siegfried Lang, Tim Sueselbeck, Christian Wolpert, Jens J Kaden, Carlos Jaramillo, Guenter Huhle, Martin Borggrefe, Karl K Haase
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  ABSTRACT: Inflammation within coronary plaques may cause an acute coronary syndrome by promoting rupture and erosion. It was the aim of this study to examine whether markers of inflammation derive from a cardiac or extracardiac source and how their levels develop over time. Blood samples were taken from patients with acute coronary syndromes (ACS) with proven atherosclerotic lesion(s) of the left coronary artery (n=13) and from control patients without coronary artery disease (n=13). Blood was taken from the femoral vein and the coronary sinus vein before and after coronary angioplasty (day 0) and on days 1 and 120. Levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-1-receptor antagonist (IL-1 ra) and soluble CD40 ligand (sCD40L) were higher in ACS patients as compared to controls and remained elevated up to day 120. In the long-term time course these markers of inflammation and plaque remodeling slightly decreased in ACS patients. There were no statistically significant differences detectable in the levels of TNF-alpha, IL-6, IL-1 beta, IL-10, IL-1 ra, sCD40L and monocyte chemoattractant protein-1 (MCP-1) in the blood of ACS patients taken from a cardiac source as compared to an extracardiac source (coronary sinus vs. femoral vein). This study demonstrates the importance of a systemic inflammatory condition in patients with ACS, in whom markers of inflammation are increased as compared to controls. During long-term follow-up the pro-inflammatory activity remains elevated in ACS patients, supporting the concept of a systemic rather than a local vascular inflammation contributing to the development of atherosclerosis.
  Clinical Chemistry and Laboratory Medicine 02/2004; 42(10):1132-9. · 2.15 Impact Factor
• Article: N-terminal pro-atrial natriuretic peptide as a biochemical marker of long-term interventional success after radiofrequency catheter ablation of paroxysmal supraventricular tachyarrhythmias.

  Martina Brueckmann, Thomas Bertsch, Ursula Hoffmann, Siegfried Lang, Jens J Kaden, Christian Wolpert, Guenter Huhle, Martin Borggrefe, Karl K Haase
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  ABSTRACT: Radiofrequency (RF) catheter ablation has been shown to be highly effective in the treatment of supraventricular tachycardias. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (B-type natriuretic peptide; BNP) are secreted by the heart mainly in response to myocardial stretch induced by volume load. The aim of the present study was to determine the time course of the N-terminal prohormone forms of ANP (NT-proANP) and BNP (NT-proBNP) in patients undergoing radiofrequency (RF) catheter ablation for paroxysmal supraventricular tachycardias. Serial blood samples were taken from 13 patients with symptomatic paroxysmal supraventricular tachycardias undergoing RF ablation and from 13 age- and gender-matched healthy controls. Blood was taken before ablation (day 0, baseline), and at day one and day 120 after ablation. Levels of NT-proANP were significantly higher before RF ablation (4862+/-726 pmol/l) as compared to day one (2021+/-220 pmol/l) and day 120 after RF ablation (2470+/-349 pmol/l) (with p<0.01 on day one and p<0.05 on day 120; n=13). The size of the left atrium decreased from 41.0+/-5.5 mm before ablation to 34.9+/-5.9 mm (n=13; p<0.05) on day 120 as measured by M-mode echocardiography. Levels of NT-proBNP showed comparable values before and on day one and day 120 after ablation and were not significantly elevated as compared to healthy controls. NT-proANP levels are increased in patients presenting with paroxysmal supraventricular tachycardias and decrease one day after radiofrequency catheter ablation, possibly reflecting a transient reduction of ANP secretion from injured myocardial cells. Lower NT-proANP levels in the long-term time course may result from reduction of atrial volume load and reconstitution of atrial architecture after successful treatment of supraventricular tachycardias. NT-proANP may serve as a useful laboratory marker to describe the long-term interventional success after RF ablation.
  Clinical Chemistry and Laboratory Medicine 02/2004; 42(8):896-902. · 2.15 Impact Factor
• Article: Blood loss from laboratory tests.

  Dirk Wisser, Klaus van Ackern, Ernst Knoll, Hermann Wisser, Thomas Bertsch
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  ABSTRACT: Laboratory tests can be an important source of blood loss in hospitals, especially for newborns and patients in intensive care. The aim of this study was to quantify blood loss for laboratory diagnostic tests in a large number of patients in a teaching hospital. We estimated blood loss by multiplying the number and volumes of sampling tubes collected from 2654 adult inpatients. We compared the number of tests per patient for all inpatients and intensive care unit patients during the first period and again in the same time period 1 year later when cumulative blood-loss volumes were being reported to physicians and educational information had been given to decrease blood loss from laboratory tests. For 95% of the patients, blood loss during hospitalization was <196 mL. The largest proportion of the blood samples was used for clinical chemical tests (median, 45%), followed by hematologic (median, 26%) and coagulation (median, 17%) tests. In the surgical and cardiovascular surgical intensive care units, however, blood gas analyses accounted for 19-34% (medians) of the use. For 5% of the patients, all undergoing intensive care, blood loss was >200 mL and for 0.7% was >600 mL during their hospital stay. Such high blood losses were observed in patients with long-term ventilation, coagulation disorders, and repeated surgery. The largest median blood loss was in patients undergoing cardiovascular surgery (median, 201 mL). The mean number of tests was 44 per inpatient before cumulative blood loss was being reported and 46 when it was being reported. Blood loss from laboratory diagnostic testing is not likely to pose a problem for most hospitalized patients. Blood loss is greater in intensive care patients and after cardiovascular surgical procedures. Reporting of the cumulative individual blood loss did not decrease blood loss for laboratory testing.
  Clinical Chemistry 10/2003; 49(10):1651-5. · 7.91 Impact Factor
• Article: Intestinal ischaemia during cardiac arrest and resuscitation: comparative analysis of extracellular metabolites by microdialysis.

  Ulrike Korth, Heiner Krieter, Christof Denz, Christoph Janke, Klaus Ellinger, Thomas Bertsch, Claudia Henn, Jochen Klein
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  ABSTRACT: Intestinal ischaemia is a major complication of shock syndromes causing translocation of bacteria and endotoxins and multiple organ failure in intensive care patients. The present study was designed to use microdialysis as a tool to monitor intestinal ischaemia after cardiac arrest and resuscitation in pigs. For this purpose, microdialysis probes were implanted in pig jejunal wall, peritoneum, skeletal muscle and brain, and interstitial fluid was obtained during circulatory arrest (induced by ventricular fibrillation) and after return of spontaneous circulation (ROSC). Cardiac arrest for 4 min caused a prolonged (60 min) reduction of blood flow in jejunal wall, muscle and brain as determined by the ethanol technique. This was accompanied by cellular damage in heart muscle and brain as indicated by increased levels of troponin-I and protein S-100, respectively. Plasma levels of glucose, lactate and choline were increased at 15-60 min following cardiac arrest. In contrast, cardiac arrest induced a rapid but variable decrease of interstitial glucose levels in all monitored organs; this decrease was followed by an increase over baseline during reperfusion. In the intestine, lactate, glutamate and choline levels were increased during ischaemia and reperfusion for 60-120 min; intestinal and peritoneal samples yielded parallel changes of lactate levels. Brain and muscle samples showed similar changes as in intestinum and peritoneum except for glutamate, which was increased in brain but not in muscle. We conclude that intestinal ischaemia occurs as a consequence of cardiac arrest and resuscitation and can be monitored by in vivo microdialysis. Comparative analysis by multi-site microdialysis reveals that the intestine is equally or even more sensitive to ischaemia than brain or muscle.
  Resuscitation 09/2003; 58(2):209-17. · 3.60 Impact Factor
• Article: Early prediction of neurological outcome after cardiopulmonary resuscitation: a multimodal approach combining neurobiochemical and electrophysiological investigations may provide high prognostic certainty in patients after cardiac arrest.

  Vera Carina Zingler, Bertram Krumm, Thomas Bertsch, Klaus Fassbender, Bernd Pohlmann-Eden
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  ABSTRACT: A reliable and reproducible method for precisely predicting the neurological outcome of patients with hypoxic-ischemic encephalopathy after cardiac arrest is urgently needed in neurological intensive care units. We prospectively investigated the predictive power of serum concentrations of neuron-specific enolase (NSE) and protein S-100B (S-100B) measured on days 1, 2, 3 and 7 as well as somatosensory-evoked potentials (SEPs) recorded within 48 h and on day 7 after cardiopulmonary resuscitation (CPR) in 27 patients (14 females, 13 males; mean age 61.3 +/- 17.3 years) with hypoxic-ischemic encephalopathy. During the first 7 days after CPR, median values of NSE and S-100B were increased in patients who remained unconscious after CPR compared to those patients who regained consciousness (significance up to < or =0.001). The best predictor of negative outcome was an NSE cutoff point > or =43 microg/l on day 2; this had a sensitivity of 90.9% and a specificity of 100%. Additional use of S-100B on day 2 did not increase sensitivity, but this could be markedly increased by combining NSE and S-100B on days 1, 3 and 7. SEPs showing bilateral loss of cortical responses identified patients who did not regain consciousness with a specificity of 100%.
  European Neurology 01/2003; 49(2):79-84. · 1.81 Impact Factor
• Article: Glycosylation processing inhibition by castanospermine prevents experimental autoimmune encephalomyelitis by interference with IL-2 receptor signal transduction.

  Silke Walter, Klaus Fassbender, Erich Gulbins, Yang Liu, Monika Rieschel, Monika Herten, Thomas Bertsch, Britta Engelhardt
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  ABSTRACT: In this study, we explored the therapeutic targets of the glycosylation processing inhibitor, castanospermine (CAST), in murine passive transfer experimental autoimmune encephalomyelitis (EAE), a model disease of multiple sclerosis. By using lymphocytic-endothelial adhesion and transmigration assays, FACScan and Western blotting, we defined the effects of CAST on expression, function and signal transduction of glycoproteins crucial in the pathophysiology of this disease. CAST prevented clinical signs of EAE and completely inhibited inflammatory CNS infiltrates associated with this disease. Here, we showed that CAST blocks antigen-induced lymphocytic activation and clonal expansion in a dose-dependent manner. Importantly, we observed that CAST strongly impairs IL-2-induced signal transduction of the IL-2 receptor. In contrast, neither expression nor binding ability of the IL-2 receptor was affected by this drug. In addition, we were able to exclude major effects of CAST on expression and function of different glycoproteins important in antigen presentation as well as lymphocytic-endothelial adhesion and transmigration. In conclusion, CAST strongly interferes in the signal transduction of the IL-2 receptor. This could explain both inhibitory effects of CAST in clonal T cell expansion and development of transfer EAE. This relatively selective pharmacological effect of CAST highlights its potential as a novel immunomodulatory approach in multiple sclerosis.
  Journal of Neuroimmunology 12/2002; 132(1-2):1-10. · 2.96 Impact Factor
• Article: Hypertonic-hyperoncotic solutions reduce the release of cardiac troponin I and s-100 after successful cardiopulmonary resuscitation in pigs.

  Heiner Krieter, Christof Denz, Christoph Janke, Thomas Bertsch, Thomas Luiz, Klaus Ellinger, Klaus Van Ackern
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  ABSTRACT: In some patients, cardiopulmonary resuscitation (CPR) can revive spontaneous circulation (ROSC). However, neurological outcome often remains poor. Hypertonic-hyperoncotic solutions (HHS) have been shown to improve microvascular conductivity after regional and global ischemia. We investigated the effect of infusion of HHS in a porcine CPR model. Cardiac arrest was induced by ventricular fibrillation. Advanced cardiac life support was begun after 4 min of nonintervention and 1 min of basic life support. Upon ROSC, the animals randomly received 125 mL of either normal saline (placebo, n = 8) or 7.2% NaCl and 10% hydroxyethyl starch 200,000/0.5 (HHS, n = 7). Myocardial and cerebral damage were assessed by serum concentrations of cardiac troponin I and astroglial protein S-100, respectively, up to 240 min after ROSC. In all animals, the levels of cardiac troponin I and S-100 increased after ROSC (P < 0.01). This increase was significantly blunted in animals that received HHS instead of placebo. The use of HHS in the setting of CPR may provide a new option in reducing cell damage in postischemic myocardial and cerebral tissues. IMPLICATIONS: Infusion of hypertonic-hyperoncotic solutions (HHS) after successful cardiopulmonary resuscitation in pigs significantly reduced the release of cardiac troponin I and cerebral protein S-100, which are sensitive and specific markers of cell damage. Treatment with HHS may provide a new option to improve the outcome of cardiopulmonary resuscitation.
  Anesthesia & Analgesia 11/2002; 95(4):1031-6, table of contents. · 3.29 Impact Factor
• Article: Influence of simvastatin, pravastatin, and BM 15.766 on neutral sterols in liver and testis of guinea pigs.

  Bernhard Lindenthal, Thomas Bertsch, Klaus Fassbender, Mark Stroick, Sandra Kühl, Dieter Lütjohann, Klaus von Bergmann
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  ABSTRACT: There is mounting evidence that specific sterol precursors of cholesterol are associated with reproductive functions. Testicular meiosis-activating sterol (T-MAS) and follicular fluid meiosis-activating-sterol (FF-MAS) are 2 cholesterol precursors found in reproductive organs of mammals, which are able to overcome meiotic arrest in vitro. This study investigates the influence of simvastatin and pravastatin, 2 inhibitors of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase, and BM 15.766, an inhibitor of 7-dehydrocholesterol reductase, on concentrations of neutral sterols in liver and testis of guinea pigs. Concentrations of T-MAS, lathosterol, and desmosterol were markedly higher in testis compared with liver. Simvastatin (150 mg/d) and pravastatin (150 mg/d and 350 mg/d) markedly reduced cholesterol precursors in liver. In contrast, T-MAS and desmosterol in testis remained unchanged, albeit other cholesterol precursors were reduced. BM 15.766 led to the accumulation of 7- and 8-dehydrocholesterol, both in liver and testis. However, concentrations of T-MAS in testis were not changed by BM 15.766. We conclude that treatment of guinea pigs with simvastatin, pravastatin, or BM 15.766, which simulates the biochemical defect of the Smith-Lemli-Opitz (SLO) syndrome, does not affect T-MAS concentrations in testis.
  Metabolism 05/2002; 51(4):492-9. · 2.66 Impact Factor
• Article: Pancreatic phospholipase A2 activity in acute pancreatitis: a prognostic marker for early identification of patients at risk.

  Johannes Aufenanger, Michael Samman, Michael Quintel, Klaus Fassbender, Wilma Zimmer, Thomas Bertsch
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  ABSTRACT: Remarkably elevated levels of phospholipase A2 (PLA2) are measurable in human blood samples in cases of acute pancreatitis. The source of the enzyme was first thought to be exclusively the pancreas, but now it is generally accepted that two isoenzymes--the pancreatic PLA2, group I, and the extrapancreatic PLA2, group II--contribute to the raised activity. In contrast to the group II-PLA2, the pancreatic PLA2 is heat-resistant for 1 hour at 60 degrees C. The catalytically inactive proenzyme of the pancreatic PLA2 can be activated by trypsin. The aim of our study was to evaluate the diagnostic value of PLA2 isoenzyme activity measurements to identify patients with severe complications in acute pancreatitis. Blood samples from patients suffering from acute pancreatitis were analyzed for catalytically active pancreatic PLA2 on day 1 and 2 of hospitalization with a modified radiometric Escherichia coli-based PLA2 assay. In 10 of 41 patients clearly elevated values of catalytically active, heat-resistant pancreatic PLA2 (7.2 to 81.2 U/l) were observed. This group of patients was characterized by severe complications (necrotizing pancreatitis, shock, sepsis, respiratory problems) of which two patients subsequently died. Patients with low or undetectable activity (<7 U/l) of pancreatic PLA2 recovered rapidly. According to these results the presence of catalytically active pancreatic PLA2 in serum is associated with severe complications of acute pancreatitis. In contrast to total serum-PLA2, the catalytic concentration of pancreatic PLA2 can serve as a prognostic marker in acute pancreatitis.
  Clinical Chemistry and Laboratory Medicine 04/2002; 40(3):293-7. · 2.15 Impact Factor
• Article: Inflammatory leukocyte infiltration in focal cerebral ischemia: unrelated to infarct size.

  Klaus Fassbender, Andreas Ragoschke, Sandra Kühl, Kristina Szabo, Marc Fatar, Walter Back, Thomas Bertsch, Stefan Kreisel, Michael Hennerici
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  ABSTRACT: An inflammatory host response in the ischemically injured brain is well documented. However, its pathophysiological relevance is uncertain. We investigated whether inflammatory leukocyte response in the ischemic brain alters infarct size. The cellular inflammatory response to cerebral ischemia in Wistar-derived rats induced by the transient occlusion of the middle cerebral artery with a thread was pharmacologically upmodulated by lipopolysaccharide (LPS) or downmodulated by continuous infusion of carboxylated sialyl Lewis(x) (sLex). The effects of such experimental modulation of focal cerebral leukocyte recruitment on the extent of the resulting infarction were assessed. Compared to control treatments, LPS strongly enhanced (540.5 +/- 504.8 vs. 94.6 +/- 60.6, p < 0.01) and sLex decreased (32.8 +/- 29.1 vs. 97.0 +/- 49.7, p < 0.05) the numbers of neutrophils at the investigated sites in cerebral ischemia. Unexpectedly, despite such marked experimental modulation of leukocyte infiltration in the ischemic brain, the extent of the resulting cerebral infarction (percent of total hemisphere) remained unchanged under these different conditions (54.5 +/- 10.8 vs. 53.0 +/- 19.1, n.s. and 50.3 +/- 18.0 vs. 57.2 +/- 10.0, n.s., respectively). The striking dissociation between the massively altered inflammatory leukocyte infiltration in the ischemic brain and the unchanged infarct outcome indicates that intracerebral inflammatory leukocyte recruitment is not a major pathogenic factor in the development of ischemic tissue damage.
  Cerebrovascular Diseases 02/2002; 13(3):198-203. · 2.72 Impact Factor
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  Available from: iiarjournals.org

  Article: Coagulation activation is associated with interleukin-6 plasma levels in patients with mechanical prosthetic heart valves.

  Volker Liebe, Jens J Kaden, Sanjay Isaaci, Martina Brueckmanni, Ursula Hoffmann, Thomas Bertsch, Martin Borggrefe, Carl-Erik Dempfle
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  ABSTRACT: The intensity of oral anticoagulant therapy in patients with mechanical heart valves is evaluated and controlled by the International Normalized Ratio (INR). However, intravascular coagulation activation can occur despite normal INR values and is related to clinical events. Here, anticoagulation efficiency was assessed by sensitive techniques and potential determinants of coagulation activation were identified. Forty patients were enrolled after they had undergone mechanical aortic valve replacement. As markers of coagulation activation, plasma concentrations of the D-dimer antigen were prospectively measured. The patients were classified into quartiles according to the D-dimer plasma antigen level. Serum concentrations of the inflammatory markers C-reactive protein (CRP) and Interleukin (IL)-6 were also assessed. The D-dimer levels varied significantly despite therapeutic INR values. In patients with high D-dimer levels, the serum concentrations of IL-6 were significantly increased (top vs. bottom quartile, median, 1.35 versus 0.80 pg/ml; p<0.05), suggestive of subclinical inflammation. There was no association between the D-dimer levels and age, sex, cardiovascular risk factors or time since valve replacement. Coagulation activation and inflammation are associated with mechanical heart valves. The D-dimer antigen and IL-6 may be more sensitive than INR and CRP to detect these states and, therefore, could prove valuable additional markers, e.g., in determining the efficacy of new anticoagulant drugs.
  In vivo (Athens, Greece) 20(3):427-30. · 1.17 Impact Factor
• Article: Temporal profile of release of interleukin-1β in neurotrauma

  Klaus Fassbender, Susanne Schneider, Thomas Bertsch, Dirk Schlueter, Marc Fatar, Andreas Ragoschke, Sandra Kühl, Udo Kischka, Michael Hennerici
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  ABSTRACT: Timing and extent of trauma-induced release of interleukin-1β (IL-1β) in extracellular fluid of the CNS were analyzed. In brain tissue perfusates obtained by in vivo microdialysis a marked release of IL-1β was unexpectedly detected within less than 60 min. At such an early stage of neurotrauma, mRNA expression of IL-1β was detected whereas immunoreactivity for the IL-1β protein was negative. Concentrations of extracellularly secreted IL-1β protein gradually increased, peaked at day 2 and decreased thereafter. Drugs acting on mononuclear phagocytes significantly modulated IL-1β secretion. This so far unrecognized acuity of IL-1β release demonstrated here, may represent a precondition for the orchestrating role of this mediator in the cascade of inflammatory host response.
  Neuroscience Letters.