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Search Results: 1 - 10 of 325241 matches for " S. Kox "
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The effects of physical exercise on plasma levels of relaxin, NTproANP, and NTproBNP in patients with ischemic heart disease
M Heringlake, T Kox, J Poeling, S Klaus, T Hanke, N Franz, F Eberhardt, H Heinze, FP Armbruster, L Bahlmann
European Journal of Medical Research , 2009, DOI: 10.1186/2047-783x-14-3-106
Abstract: The insulin-like polypeptide relaxin (RLX), formerly known as a pregnancy hormone [1], has gained interest as a potential humoral mediator in human heart failure [2]. Dschietzig and coworkers [3] have shown that the plasma levels of RLX are increased in relation to the severity of myocardial dysfunction, that the heart is a relevant source of RLX during cardiac failure, and that plasma RLX concentrations are related to left ventricular filling pressures. Comparably, Fisher and coworkers observed high RLX levels in patients with heart failure [4]. In contrast, Kupari and coworkers [5] failed to detect increased plasma RLX levels in patients with aortic valve disease but confirmed that the heart is capable of producing RLX during heart failure states.Krueger et al. analyzed the effects of physical exercise on plasma RLX levels in patients with heart failure in comparison with healthy controls and observed that plasma RLX levels neither were different between groups nor changed during physical exercise [6]. However, this study investigated a heterogeneous group of heart failure patients including subjects with idiopathic cardiomyopathy as well as patients with ischemic heart disease. Additionally the study did not relate RLX levels to hemodynamics and the plasma concentrations of natriuretic peptides.The present study was thus designed to determine the effects of physical exercise (bicycle ergometry) on the plasma levels of RLX and N-terminal pro A and B type natriuretic peptides (NTproANP and NTproB-NP, respectively) as established humoral markers for the severity of myocardial dysfunction in a homogeneous group of patients with ischemic heart disease of different severity. Additionally, the relationsship between cardiac power output at maximal charge and the respective hormone levels were analyzed.The investigation conforms with the principles outlined in the Declaration of Helsinki. Following approval by the institutional review board and written informed consent, 4
G$^0$ Electronics and Data Acquisition (Forward-Angle Measurements)
D. Marchand,J. Arvieux,L. Bimbot,A. Biselli,J. Bouvier,H. Breuer,R. Clark,J. -C. Cuzon,M. Engrand,R. Foglio,C. Furget,X. Grave,B. Guillon,H. Guler,P. M. King,S. Kox,J. Kuhn,Y. Ky,J. Lachniet,J. Lenoble,E. Liatard,J. Liu,E. Munoz,J. Pouxe,G. Quéméner,B. Quinn,J. -S. Réal,O. Rossetto,R. Sellem
Physics , 2007, DOI: 10.1016/j.nima.2007.11.028
Abstract: The G$^0$ parity-violation experiment at Jefferson Lab (Newport News, VA) is designed to determine the contribution of strange/anti-strange quark pairs to the intrinsic properties of the proton. In the forward-angle part of the experiment, the asymmetry in the cross section was measured for $\vec{e}p$ elastic scattering by counting the recoil protons corresponding to the two beam-helicity states. Due to the high accuracy required on the asymmetry, the G$^0$ experiment was based on a custom experimental setup with its own associated electronics and data acquisition (DAQ) system. Highly specialized time-encoding electronics provided time-of-flight spectra for each detector for each helicity state. More conventional electronics was used for monitoring (mainly FastBus). The time-encoding electronics and the DAQ system have been designed to handle events at a mean rate of 2 MHz per detector with low deadtime and to minimize helicity-correlated systematic errors. In this paper, we outline the general architecture and the main features of the electronics and the DAQ system dedicated to G$^0$ forward-angle measurements.
Mild hypothermia after near drowning in twin toddlers
Ortrud Hein, Andreas Triltsch, Christoph von Buch, Wolfgang J Kox, Claudia Spies
Critical Care , 2004, DOI: 10.1186/cc2926
Abstract: Two twin toddlers (a boy and girl, aged 2 years and 3 months) suffered hypothermic near drowning with protracted cardiac arrest and aspiration. The girl was treated with mild hypothermia for 72 hours and developed acute respiratory dysfunction syndrome and sepsis. She recovered without neurological deficit. The boy's treatment was conducted under normothermia without further complications. He developed an apallic syndrome.Although the twin toddlers experienced the same near drowning accident together, the outcomes with respect to neurological status and postinjury complications were completely different. One of the factors that possibly influenced the different postinjury course might have been prolonged mild hypothermia.Of drowning and near drowning victims who are younger than 20 years, 63–68% are 0–5 years old [1,2]. Of submersion events in the age group 1–4 years, 56% occurred in artificial pools [3]. Death from drowning is the second leading cause of accidental death in children [4], and one-third of all survivors have neurological damage [4]. Hypothermia frequently accompanies submersion accidents, especially in children with a relatively large ratio of surface area to body mass [3]. Mild hypothermia (32–34°C) reduces oxygen consumption by 7% per 1°C decrease in temperature, and reduces cerebral blood flow and cerebral intracranial pressure [5-7]. Temperature under 28°C leads to cardiocirculatory depression and finally cardiac arrest [3]. Hypoxaemia and capillary leak develop due to apnoea, regardless of whether aspiration occurs [3]. The degree of cerebral protection that can be expected due to hypothermia depends, among other factors, on the amount of time that elapses before induction of mild hypothermia [1,3,6]. Induced mild hypothermia for cerebral protection after near drowning accidents has yielded controversial results in terms of mortality and neurological outcome [1,3,8]. However, induced mild hypothermia after cardiac arrest has led to improved neur
Xenon prevents cellular damage in differentiated PC-12 cells exposed to hypoxia
Christian Petzelt, Per Blom, Wolfgang Schmehl, Jana Müller, Wolfgang J Kox
BMC Neuroscience , 2004, DOI: 10.1186/1471-2202-5-55
Abstract: Pheochromocytoma cells differentiated by addition of nerve growth factor were placed in a N2-saturated atmosphere, a treatment that induced release of dopamine, reaching a maximum after 30 min. By determining extracellular lactate dehydrogenase concentration as marker for concomitant cellular damage, a substantial increase of enzymatic activity was found for N2-treated cells. Replacement of N2 by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release. Intracellular buffering of Ca2+ using the Ca-chelator 1, 2-bis(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl) ester (BAPTA) reduced the neuroprotective effect of xenon indicating the essential participation of intracellular Ca2+-ions in the process of xenon-induced neuroprotection.The results presented demonstrate the outstanding property of xenon to protect neuron-like cells in a hypoxic situation.Originally, hypoxia/ischemia-induced alterations in neuronal function have been attributed to be an over-release of neurotransmitters, including dopamine and glutamate. Many studies have been performed on the mechanisms of glutamate-induced neuronal damage [1,2] but relatively few have investigated the hypoxia-induced damage in dopaminergic neurons [3-6]. In recent years several lines of evidence have suggested that effects other than excitotoxic mechanisms may also participate in hypoxia-induced cell damage such as cortical spreading depression [7,8]. Rat pheochromocytoma (PC-12) cells are catecholaminergic, excitable cells that have been widely used as an in vitro model for neuronal cells [9] possessing both D1- and D2-dopamine receptors [10]. In these cells hypoxia causes a transient release of dopamine resulting from a complex cellular response consisting of increased dopamine release and reduced uptake rate. Such increased dopamine concentration has been shown to be associated with cellular damage indicated b
Local solid-state modification of nanopore surface charges
Ronald Kox,Stella Deheryan,Chang Chen,Nima Arjmandi,Liesbet Lagae,Gustaaf Borghs
Physics , 2012, DOI: 10.1088/0957-4484/21/33/335703
Abstract: The last decade, nanopores have emerged as a new and interesting tool for the study of biological macromolecules like proteins and DNA. While biological pores, especially alpha-hemolysin, have been promising for the detection of DNA, their poor chemical stability limits their use. For this reason, researchers are trying to mimic their behaviour using more stable, solid-state nanopores. The most successful tools to fabricate such nanopores use high energy electron or ions beams to drill or reshape holes in very thin membranes. While the resolution of these methods can be very good, they require tools that are not commonly available and tend to damage and charge the nanopore surface. In this work, we show nanopores that have been fabricated using standard micromachning techniques together with EBID, and present a simple model that is used to estimate the surface charge. The results show that EBID with a silicon oxide precursor can be used to tune the nanopore surface and that the surface charge is stable over a wide range of concentrations.
Effects of Vagus Nerve Stimulation and Vagotomy on Systemic and Pulmonary Inflammation in a Two-Hit Model in Rats
Matthijs Kox, Michiel Vaneker, Johannes G. van der Hoeven, Gert-Jan Scheffer, Cornelia W. Hoedemaekers, Peter Pickkers
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034431
Abstract: Pulmonary inflammation contributes to ventilator-induced lung injury. Sepsis-induced pulmonary inflammation (first hit) may be potentiated by mechanical ventilation (MV, second hit). Electrical stimulation of the vagus nerve has been shown to attenuate inflammation in various animal models through the cholinergic anti-inflammatory pathway. We determined the effects of vagotomy (VGX) and vagus nerve stimulation (VNS) on systemic and pulmonary inflammation in a two-hit model. Male Sprague-Dawley rats were i.v. administered lipopolysaccharide (LPS) and subsequently underwent VGX, VNS or a sham operation. 1 hour following LPS, MV with low (8 mL/kg) or moderate (15 mL/kg) tidal volumes was initiated, or animals were left breathing spontaneously (SP). After 4 hours of MV or SP, rats were sacrificed. Cytokine and blood gas analysis was performed. MV with 15, but not 8 mL/kg, potentiated the LPS-induced pulmonary pro-inflammatory cytokine response (TNF-α, IL-6, KC: p<0.05 compared to LPS-SP), but did not affect systemic inflammation or impair oxygenation. VGX enhanced the LPS-induced pulmonary, but not systemic pro-inflammatory cytokine response in spontaneously breathing, but not in MV animals (TNF-α, IL-6, KC: p<0.05 compared to SHAM), and resulted in decreased pO2 (p<0.05 compared to sham-operated animals). VNS did not affect any of the studied parameters in both SP and MV animals. In conclusion, MV with moderate tidal volumes potentiates the pulmonary inflammatory response elicited by systemic LPS administration. No beneficial effects of vagus nerve stimulation performed following LPS administration were found. These results questions the clinical applicability of stimulation of the cholinergic anti-inflammatory pathway in systemically inflamed patients admitted to the ICU where MV is initiated.
Altered immune parameters in chronic alcoholic patients at the onset of infection and of septic shock
Vera von Dossow, Corinna Schilling, Stefan Beller, Ortrud Hein, Christian von Heymann, Wolfgang J Kox, Claudia D Spies
Critical Care , 2004, DOI: 10.1186/cc2911
Abstract: Twenty-eight patients from a cohort of fifty-six with either pneumonia or peritonitis and subsequent septic shock were selected. Fourteen patients were chronic alcoholics whereas fourteen were nonalcoholic patients. Chronic alcoholic patients met criteria (Diagnostic and Statistical Manual of Mental Disorders IV, of the American Psychiatric Association) for alcohol abuse or dependence. Measurements were performed during the onset of infection (within 24 hours after the onset of infection), in early septic shock (within 12 hours after onset of septic shock) and in late septic shock (72 hours after the onset). Blood measurements included proinflammatory and anti-inflammatory cytokines.Chronic alcoholic patients exhibited significantly lower plasma levels of IL-8 (P < 0.010) during the onset of infection than did matched nonalcoholic patients. In early septic shock, chronic alcoholic patients had significantly decreased levels of IL-1β (P < 0.015), IL-6 (P < 0.016) and IL-8 (P < 0.010). The anti-inflammatory parameters IL-10 and tumour necrosis factor receptors I and II did not differ between alcoholic and nonalcoholic patients.At the onset of infection and during early septic shock, chronic alcoholic patients had lower levels of proinflammatory immune parameters than did nonalcoholic patients. Therefore, immunomodulatory therapy administered early may be considered in chronic alcoholic patients at the onset of an infection because of their altered proinflammatory immune response.Chronic alcoholic patients have a twofold to fivefold increased risk for postoperative morbidity after surgery as compared with nonalcoholic patients [1,2]. As a result of this increased postoperative morbidity, intensive care treatment and overall hospital stay are prolonged [1,2]. Among all complications, infections are the most serious and are associated with a worse outcome [1-3].Prolonged and excessive consumption of alcohol has been shown to predispose to a variety of infectious complica
Biomarkers associated with delirium in critically ill patients and their relation with long-term subjective cognitive dysfunction; indications for different pathways governing delirium in inflamed and noninflamed patients
Mark van den Boogaard, Matthijs Kox, Kieran L Quinn, Theo van Achterberg, Johannes G van der Hoeven, Lisette Schoonhoven, Peter Pickkers
Critical Care , 2011, DOI: 10.1186/cc10598
Abstract: In an exploratory observational study, we included 100 ICU patients with or without delirium and with ("inflamed") and without ("noninflamed") infection/systemic inflammatory response syndrome (SIRS). Delirium was diagnosed by using the confusion-assessment method-ICU (CAM-ICU). Within 24 hours after the onset of delirium, blood was obtained for biomarker analysis. No differences in patient characteristics were found between delirious and nondelirious patients. To determine associations between biomarkers and delirium, univariate and multivariate logistic regression analyses were performed. Eighteen months after ICU discharge, a cognitive-failure questionnaire was distributed to the ICU survivors.In total, 50 delirious and 50 nondelirious patients were included. We found that IL-8, MCP-1, procalcitonin (PCT), cortisol, and S100-β were significantly associated with delirium in inflamed patients (n = 46). In the noninflamed group of patients (n = 54), IL-8, IL-1ra, IL-10 ratio Aβ1-42/40, and ratio AβN-42/40 were significantly associated with delirium. In multivariate regression analysis, IL-8 was independently associated (odds ratio, 9.0; 95% confidence interval (CI), 1.8 to 44.0) with delirium in inflamed patients and IL-10 (OR 2.6; 95% CI 1.1 to 5.9), and Aβ1-42/40 (OR, 0.03; 95% CI, 0.002 to 0.50) with delirium in noninflamed patients. Furthermore, levels of several amyloid-β forms, but not human Tau or S100-β, were significantly correlated with self-reported cognitive impairment 18 months after ICU discharge, whereas inflammatory markers were not correlated to impaired long-term cognitive function.In inflamed patients, the proinflammatory cytokine IL-8 was associated with delirium, whereas in noninflamed patients, antiinflammatory cytokine IL-10 and Aβ1-42/40 were associated with delirium. This suggests that the underlying mechanism governing the development of delirium in inflamed patients differs from that in noninflamed patients. Finally, elevated levels of amy
IFN-γ-Stimulated Neutrophils Suppress Lymphocyte Proliferation through Expression of PD-L1
Stan de Kleijn, Jeroen D. Langereis, Jenneke Leentjens, Matthijs Kox, Mihai G. Netea, Leo Koenderman, Gerben Ferwerda, Peter Pickkers, Peter W. M. Hermans
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072249
Abstract: During systemic inflammation different neutrophil subsets are mobilized to the peripheral blood. These neutrophil subsets can be distinguished from normal circulating neutrophils (CD16bright/CD62Lbright), based on either an immature CD16dim/CD62Lbright or a CD16bright/CD62Ldim phenotype. Interestingly, the latter neutrophil subset is known to suppress lymphocyte proliferation ex vivo, but how neutrophils become suppressive is unknown. We performed transcriptome analysis on the different neutrophil subsets to identify changes in mRNA expression that are relevant for their functions. Neutrophil subsets were isolated by fluorescence-activated cell sorting from blood of healthy volunteers that were administered a single dose of lipopolysaccharide (2 ng/kg i.v.) and the transcriptome was determined by microarray analysis. Interestingly, the CD16bright/CD62Ldim suppressive neutrophils showed an interferon-induced transcriptome profile. More importantly, IFN-γ, but not IFN-α or IFN-β stimulated neutrophils, acquired the capacity to suppress lymphocyte proliferation through the expression of programmed death ligand 1 (PD-L1). These data demonstrate that IFN-γ-induced expression of PD-L1 on neutrophils enables suppression of lymphocyte proliferation. Specific stimulation of neutrophils present at the inflammatory sites might therefore have a pivotal role in regulating lymphocyte-mediated inflammation and autoimmune disease.
Transcriptome Kinetics of Circulating Neutrophils during Human Experimental Endotoxemia
Stan de Kleijn, Matthijs Kox, Iziah Edwin Sama, Janesh Pillay, Angela van Diepen, Martijn A. Huijnen, Johannes G. van der Hoeven, Gerben Ferwerda, Peter W. M. Hermans, Peter Pickkers
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038255
Abstract: Polymorphonuclear cells (neutrophils) play an important role in the systemic inflammatory response syndrome and the development of sepsis. These cells are essential for the defense against microorganisms, but may also cause tissue damage. Therefore, neutrophil numbers and activity are considered to be tightly regulated. Previous studies have investigated gene transcription during experimental endotoxemia in whole blood and peripheral blood mononuclear cells. However, the gene transcription response of the circulating pool of neutrophils to systemic inflammatory stimulation in vivo is currently unclear. We examined neutrophil gene transcription kinetics in healthy human subjects (n = 4) administered a single dose of endotoxin (LPS, 2 ng/kg iv). In addition, freshly isolated neutrophils were stimulated ex vivo with LPS, TNFα, G-CSF and GM-CSF to identify stimulus-specific gene transcription responses. Whole transcriptome microarray analysis of circulating neutrophils at 2, 4 and 6 hours after LPS infusion revealed activation of inflammatory networks which are involved in signaling of TNFα and IL-1α and IL-1β. The transcriptome profile of inflammatory activated neutrophils in vivo reflects extended survival and regulation of inflammatory responses. These changes in neutrophil transcriptome suggest a combination of early activation of circulating neutrophils by TNFα and G-CSF and a mobilization of young neutrophils from the bone marrow.
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