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Gerd Schmitz - One of the best experts on this subject based on the ideXlab platform.
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Polymorphisms in the Lipopolysaccharide-Binding Protein and bactericidal/permeability-increasing Protein in patients with myocardial infarction.
Clinical chemistry and laboratory medicine, 2002Co-Authors: Jaroslav A. Hubacek, Gerd Schmitz, Jan Pitha, Zdena Škodová, Vera Adamkova, I. Podrapska, Rudolf PoledneAbstract:Gram-negative bacterial infection, namely Chlamydia pneumoniae has been recently discussed as a risk factor for myocardial infarction. The Lipopolysaccharide-Binding Protein (LBP) and the bactericidal/permeability-increasing Protein (BPI) play a role in the processes leading to recognition and neutralisation of the Chlamydia pneumoniae and their endotoxins Lipopolysaccharides (LPS). LPS interact with plasma LBP, and LBP-LPS complex activates monocytes/macrophages, which can influence the atherosclerotic process. BPI is cytotoxic for Gram-negative bacteria and BPI-LPS complexes do not activate monocytes. We have analysed the polymorphisms in the LBP gene (Gly98-->Cys; Pro436-->Leu) and BPI gene (Lys216-->Glu; PstI polymorphism in intron-5; G545-->C) in 313 patients after myocardial infarction (MI) and in 302 control individuals. Genotype frequencies in the LBP gene and BPI gene did not differ between MI patients and control individuals. Our findings suggest that LBP and BPI polymorphisms do not influence the risk of MI.
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gene variants of the bactericidal permeability increasing Protein and Lipopolysaccharide Binding Protein in sepsis patients gender specific genetic predisposition to sepsis
Critical Care Medicine, 2001Co-Authors: Jaroslav A. Hubacek, Frank Stüber, D. Fröhlich, Malte Book, Silke Wetegrove, Mirko Ritter, Gregor Rothe, Gerd SchmitzAbstract:ObjectivesTo determine whether the genotype frequencies of the five bi-allelic polymorphisms in the bactericidal/permeability increasing Protein (BPI) (Lys216 → Glu;Pst I polymorphism in intron 5; silent mutation G545 → C) and the Lipopolysaccharide Binding Protein (LBP) (Cys98 → Gly; Pro436 → Leu)
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Gene variants of the bactericidal/permeability increasing Protein and Lipopolysaccharide Binding Protein in sepsis patients: Gender-specific genetic predisposition to sepsis
Critical care medicine, 2001Co-Authors: Jaroslav A. Hubacek, Frank Stüber, D. Fröhlich, Malte Book, Silke Wetegrove, Mirko Ritter, Gregor Rothe, Gerd SchmitzAbstract:ObjectivesTo determine whether the genotype frequencies of the five bi-allelic polymorphisms in the bactericidal/permeability increasing Protein (BPI) (Lys216 → Glu;Pst I polymorphism in intron 5; silent mutation G545 → C) and the Lipopolysaccharide Binding Protein (LBP) (Cys98 → Gly; Pro436 → Leu)
Christian F. Poets - One of the best experts on this subject based on the ideXlab platform.
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Lipopolysaccharide-Binding Protein in noninfected neonates and those with suspected early-onset bacterial infection
Journal of Perinatology, 2006Co-Authors: Thorsten W. Orlikowsky, C Trüg, Felix Neunhoeffer, M Deperschmidt, M Eichner, Christian F. PoetsAbstract:Objectives: To investigate postnatal Lipopolysaccharide-Binding Protein (LBP) kinetics in term neonates and to test its diagnostic accuracy for early-onset bacterial infection (EOBI). Study design: A total of 99 neonates with clinical and serological signs of EOBI comprised the study group; 198 neonates with risk factors, but without EOBI, served as controls. LBP, C-reactive Protein (CRP) and interleukin-8 (IL-8) were determined. Results: LBP in the noninfected group increased until 24 h after birth ( P
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Lipopolysaccharide-Binding Protein in noninfected neonates and those with suspected early-onset bacterial infection.
Journal of perinatology : official journal of the California Perinatal Association, 2006Co-Authors: Thorsten W. Orlikowsky, C Trüg, Felix Neunhoeffer, M Deperschmidt, M Eichner, Christian F. PoetsAbstract:Lipopolysaccharide-Binding Protein in noninfected neonates and those with suspected early-onset bacterial infection
Jaroslav A. Hubacek - One of the best experts on this subject based on the ideXlab platform.
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Polymorphisms in the Lipopolysaccharide-Binding Protein and bactericidal/permeability-increasing Protein in patients with myocardial infarction.
Clinical chemistry and laboratory medicine, 2002Co-Authors: Jaroslav A. Hubacek, Gerd Schmitz, Jan Pitha, Zdena Škodová, Vera Adamkova, I. Podrapska, Rudolf PoledneAbstract:Gram-negative bacterial infection, namely Chlamydia pneumoniae has been recently discussed as a risk factor for myocardial infarction. The Lipopolysaccharide-Binding Protein (LBP) and the bactericidal/permeability-increasing Protein (BPI) play a role in the processes leading to recognition and neutralisation of the Chlamydia pneumoniae and their endotoxins Lipopolysaccharides (LPS). LPS interact with plasma LBP, and LBP-LPS complex activates monocytes/macrophages, which can influence the atherosclerotic process. BPI is cytotoxic for Gram-negative bacteria and BPI-LPS complexes do not activate monocytes. We have analysed the polymorphisms in the LBP gene (Gly98-->Cys; Pro436-->Leu) and BPI gene (Lys216-->Glu; PstI polymorphism in intron-5; G545-->C) in 313 patients after myocardial infarction (MI) and in 302 control individuals. Genotype frequencies in the LBP gene and BPI gene did not differ between MI patients and control individuals. Our findings suggest that LBP and BPI polymorphisms do not influence the risk of MI.
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gene variants of the bactericidal permeability increasing Protein and Lipopolysaccharide Binding Protein in sepsis patients gender specific genetic predisposition to sepsis
Critical Care Medicine, 2001Co-Authors: Jaroslav A. Hubacek, Frank Stüber, D. Fröhlich, Malte Book, Silke Wetegrove, Mirko Ritter, Gregor Rothe, Gerd SchmitzAbstract:ObjectivesTo determine whether the genotype frequencies of the five bi-allelic polymorphisms in the bactericidal/permeability increasing Protein (BPI) (Lys216 → Glu;Pst I polymorphism in intron 5; silent mutation G545 → C) and the Lipopolysaccharide Binding Protein (LBP) (Cys98 → Gly; Pro436 → Leu)
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Gene variants of the bactericidal/permeability increasing Protein and Lipopolysaccharide Binding Protein in sepsis patients: Gender-specific genetic predisposition to sepsis
Critical care medicine, 2001Co-Authors: Jaroslav A. Hubacek, Frank Stüber, D. Fröhlich, Malte Book, Silke Wetegrove, Mirko Ritter, Gregor Rothe, Gerd SchmitzAbstract:ObjectivesTo determine whether the genotype frequencies of the five bi-allelic polymorphisms in the bactericidal/permeability increasing Protein (BPI) (Lys216 → Glu;Pst I polymorphism in intron 5; silent mutation G545 → C) and the Lipopolysaccharide Binding Protein (LBP) (Cys98 → Gly; Pro436 → Leu)
José María Moreno-navarrete - One of the best experts on this subject based on the ideXlab platform.
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Adipocyte Lipopolysaccharide Binding Protein (LBP) is linked to a specific lipidomic signature.
Obesity (Silver Spring Md.), 2016Co-Authors: José María Moreno-navarrete, Francisco Ortega, Wifredo Ricart, Mariona Jové, Teresa Padró, Jordi Boada, Reinald Pamplona, Lina Badimon, Manuel Portero-otin, José Manuel Fernández-realAbstract:Objective Lipopolysaccharide Binding Protein (LBP) is part of a family of structurally and functionally related lipid transfer Proteins. This study aimed to investigate the associations of LBP with the lipid composition of human adipose tissue. Methods Lipidomic analysis was performed in whole adipose tissue. To validate the associations found, LBP was knocked down (KD) in 3T3-L1 adipocytes, and lipidomic profile was evaluated by nontargeted lipidomics. Results LBP gene expression was negatively associated with phosphatidylcholine, phosphatidylserine, and sphingomyelin relative abundance in vivo. LBP expression was also decreased in those samples with the highest docosahexanoic content, implicated in the resolution of inflammation. The KD of LBP (by ∼70%) led to sharp changes in the lipidome of adipocytes. Of note, specific plasmalogen species PE(O-16:0/22:5), PE(38:2), odd chain glycerolipids, and cholesteryl linoleate were upregulated by LBP KD. In contrast, GM3 gangliosides, several ceramides, a triacylglycerol potentially containing arachidonate, and cholesteryl palmitate were downregulated by LBP KD. Conclusions LBP seems to play a role in the regulation of lipid composition of adipose tissue linked to resilience to inflammation.
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Lipopolysaccharide-Binding Protein is a negative regulator of adipose tissue browning in mice and humans
Diabetologia, 2016Co-Authors: Aleix Gavaldà-navarro, José Manuel Fernández-real, José María Moreno-navarrete, Tania Quesada-lópez, Montserrat Cairó, Marta Giralt, Francesc VillarroyaAbstract:Aims/hypothesis Adipocyte Lipopolysaccharide-Binding Protein (LBP) biosynthesis is associated with obesity-induced adipose tissue dysfunction. Our purpose was to study the role of LBP in regulating the browning of adipose tissue.
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A role for adipocyte-derived Lipopolysaccharide-Binding Protein in inflammation- and obesity-associated adipose tissue dysfunction.
Diabetologia, 2013Co-Authors: José María Moreno-navarrete, Francisco Ortega, Matteo Serino, Elodie Luche, Xavier Escoté, Mark Campbell, Marie-caroline Michalski, Martine Laville, Gemma Xifra, Pere DomingoAbstract:Aims/hypothesis Circulating Lipopolysaccharide-Binding Protein (LBP) is an acute-phase reactant known to be increased in obesity. We hypothesised that LBP is produced by adipose tissue (AT) in association with obesity.
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Serum Lipopolysaccharide-Binding Protein as a marker of atherosclerosis
Atherosclerosis, 2013Co-Authors: Marta Serrano, Francisco Ortega, José María Moreno-navarrete, Wifredo Ricart, Gemma Xifra, Josep Puig, María Moreno, Ester Guerra, José Manuel Fernández-realAbstract:Abstract Background Recently, serum Lipopolysaccharide-Binding Protein (LBP) has been closely associated with coronary artery disease. Here, we aimed to investigate the possible relationship between serum LBP and markers of atherosclerosis. Methods Serum LBP and carotid intima media thickness (C-IMT) were measured in 332 subjects (101 men and 231 women) who were recruited from an ongoing multicenter project. Results Serum LBP was significantly associated with obesity [BMI, fat mass and waist circumference ( r > 0.38, p r = 0.36, p r = 0.50, p r = 0.27, p β = 0.16; p = 0.001) contributed independently to C-IMT variance, after controlling for the effects of age, gender, BMI and hsCRP. Of note, circulating LBP was found to be increased in the population with carotid plaque ( n = 50; 32.7 ± 12.5 vs 28.7 ± 10.7; p = 0.021). Conclusion The consistent association between serum LBP and the carotid intima media thickness, a widely used atherosclerosis marker, reveals serum LBP as a putative factor related to atherosclerosis.
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Circulating Lipopolysaccharide-Binding Protein (LBP) as a marker of obesity-related insulin resistance
International journal of obesity (2005), 2011Co-Authors: José María Moreno-navarrete, F. Ortega, Matteo Serino, Elodie Luche, Aurélie Waget, Gerard Pardo, Javier Salvador, Wifredo Ricart, Gema Frühbeck, Rémy BurcelinAbstract:Circulating Lipopolysaccharide-Binding Protein (LBP) as a marker of obesity-related insulin resistance
Metka Derganc - One of the best experts on this subject based on the ideXlab platform.
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Diagnostic accuracy of Lipopolysaccharide-Binding Protein for predicting bacteremia/clinical sepsis in children with febrile neutropenia: comparison with interleukin-6, procalcitonin, and C-reactive Protein.
Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer, 2013Co-Authors: L Kitanovski, Sergej Hojker, Janez Jazbec, Metka DergancAbstract:Purpose In febrile neutropenia (FN), no reliable marker has been identified to discriminate between severe infection and other causes of fever early in the clinical course. Since Lipopolysaccharide-Binding Protein (LBP) has proven to be an accurate biomarker of bacteremia/clinical sepsis in critically ill non-immunocompromised infants and children, we performed a prospective study to determine the diagnostic accuracy of LBP in children with FN.
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Neutrophil and monocyte CD64 indexes, Lipopolysaccharide-Binding Protein, procalcitonin and C-reactive Protein in sepsis of critically ill neonates and children.
Intensive care medicine, 2009Co-Authors: Mojca Groselj-grenc, Maja Pavcnik-arnol, T Gmeiner-stopar, Alojz Ihan, Andreja Nataša Kopitar, Metka DergancAbstract:Objective To compare the diagnostic accuracy of neutrophil and monocyte CD64 indexes (CD64in and CD64im) for sepsis in critically ill neonates and children with that of Lipopolysaccharide-Binding Protein (LBP), procalcitonin (PCT) and C-reactive Protein (CRP).
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Lipopolysaccharide-Binding Protein, Lipopolysaccharide, and soluble CD14 in sepsis of critically ill neonates and children
Intensive Care Medicine, 2007Co-Authors: Maja Pavcnik-arnol, Sergej Hojker, Metka DergancAbstract:Objective To compare the diagnostic accuracy of Lipopolysaccharide-Binding Protein (LBP) for sepsis in critically ill neonates and children with the two markers participating in the same inflammatory pathway, Lipopolysaccharide and soluble CD14.
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Lipopolysaccharide-Binding Protein in critically ill neonates and children with suspected infection: comparison with procalcitonin, interleukin-6, and C-reactive Protein
Intensive care medicine, 2004Co-Authors: Maja Pavcnik-arnol, Sergej Hojker, Metka DergancAbstract:Objective To evaluate markers of infection in critically ill neonates and children, comparing Lipopolysaccharide-Binding Protein (LBP) with procalcitonin (PCT), interleukin-6 (IL-6), and C-reactive Protein (CRP).