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Manuel Castro Cabezas - One of the best experts on this subject based on the ideXlab platform.
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Abstract 17598: Inflammatory Effect of Fasting and Postprandial Triglycerides by Leukocyte Activation
Circulation, 2016Co-Authors: Benjamin Burggraaf, B. Klop, G.-j. M. Van De Geijn, A. Alipour, Marijke A. De Vries, Anho Liem, Peter De Man, Manuel Castro CabezasAbstract:Introduction: Atherosclerosis is characterized by systemic inflammation in which the Activation of Leukocytes plays a crucial role. While hypertriglyceridemia is an atherogenic condition, the underlying mechanisms have not been well defined. We aimed to evaluate the effect of triglycerides (TGs) on Leukocyte Activation. Methods: Volunteers (n=196) attended the outpatient clinic for fasting blood tests. Oral fat loading tests (n=36) were carried out to evaluate postprandial inflammation. For in vitro experiments, freshly drawn blood samples from 9 healthy volunteers were incubated with different TG emulsions: Lipoplus, Lipofundin and Intralipid and compared to LPS as positive control. Leukocyte Activation markers were measured using the flow cytometer. Results: The mean age of the total cohort was 56.7±16.5 years, 49.5% was male. Mean fasting TGs were 1.58±0.96 mmol/L. Fasting TGs were associated with monocyte CD11b (Spearman’s rho:0.29), granulocyte CD11b (r:0.30) and granulocyte CD66b (r:0.29). Significant associations were also found with HDLC (r:-0.38) and apoB (r:0.28; p Conclusions: This study provides evidence for a role of TGs in Leukocyte Activation, most likely depending on the composition of the TG-rich particles. These inflammatory effects may be blunted by statins. Our data contribute to the understanding of the atherogenicity of TG-rich lipoproteins.
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Coronary Leukocyte Activation in relation to progression of coronary artery disease
Frontiers of medicine, 2016Co-Authors: Marijke A. De Vries, A. Alipour, Noelle Van Der Meulen, Anho Liem, Erwin Birnie, A. Westzaan, Selvetta Van Santen, Ellen Van Der Zwan, Manuel Castro CabezasAbstract:Leukocyte Activation has been linked to atherogenesis, but there is little in vivo evidence for its role in the progression of atherosclerosis. We evaluated the predictive value for progression of coronary artery disease (CAD) of Leukocyte Activation markers in the coronary circulation. Monocyte and neutrophil CD11b, neutrophil CD66b expression and intracellular neutrophil myeloperoxidase (MPO) in the coronary arteries were determined by flow cytometry in patients undergoing coronary angiography. The primary outcome included fatal and nonfatal myocardial infarction or arterial vascular intervention due to unstable angina pectoris. In total 99 subjects who were included, 70 had CAD at inclusion (26 patients had single-vessel disease, 18 patients had twovessel disease and 26 patients had three-vessel disease). The median follow-up duration was 2242 days (interquartile range: 2142-2358). During follow-up, 13 patients (13%) developed progression of CAD. Monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO measured in blood obtained from the coronary arteries were not associated with the progression of CAD. These data indicate that coronary monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO do not predict the risk of progression of CAD.
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PS13 - 4. Gender differences in glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls
Nederlands Tijdschrift voor Diabetologie, 2013Co-Authors: Marijke A. De Vries, B. Klop, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Van Miltenburg, A. Alipour, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Atherosclerosis in type 2 diabetes mellitus (T2DM) and insulin resistance (IR) is characterized by a chronic inflammatory response in which Activation of Leukocytes is mandatory. Acute and chronic hyperglycemia may be involved in this Leukocyte Activation. Female T2DM patients have more severe atherosclerosis than male diabetics and differences in inflammation may be responsible for this observation.
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Leukocyte Activation by Triglyceride-Rich Lipoproteins
Arteriosclerosis thrombosis and vascular biology, 2008Co-Authors: A. Alipour, Antonie J.h.h.m. Van Oostrom, Alisa Izraeljan, C. Verseyden, Jennifer Collins, Keith N. Frayn, Thijs W.m. Plokker, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Objective— Postprandial lipemia has been linked to atherosclerosis and inflammation. Because Leukocyte Activation is obligatory for atherogenesis, Leukocyte Activation by triglyceride-rich lipoprot...
A. Alipour - One of the best experts on this subject based on the ideXlab platform.
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Abstract 17598: Inflammatory Effect of Fasting and Postprandial Triglycerides by Leukocyte Activation
Circulation, 2016Co-Authors: Benjamin Burggraaf, B. Klop, G.-j. M. Van De Geijn, A. Alipour, Marijke A. De Vries, Anho Liem, Peter De Man, Manuel Castro CabezasAbstract:Introduction: Atherosclerosis is characterized by systemic inflammation in which the Activation of Leukocytes plays a crucial role. While hypertriglyceridemia is an atherogenic condition, the underlying mechanisms have not been well defined. We aimed to evaluate the effect of triglycerides (TGs) on Leukocyte Activation. Methods: Volunteers (n=196) attended the outpatient clinic for fasting blood tests. Oral fat loading tests (n=36) were carried out to evaluate postprandial inflammation. For in vitro experiments, freshly drawn blood samples from 9 healthy volunteers were incubated with different TG emulsions: Lipoplus, Lipofundin and Intralipid and compared to LPS as positive control. Leukocyte Activation markers were measured using the flow cytometer. Results: The mean age of the total cohort was 56.7±16.5 years, 49.5% was male. Mean fasting TGs were 1.58±0.96 mmol/L. Fasting TGs were associated with monocyte CD11b (Spearman’s rho:0.29), granulocyte CD11b (r:0.30) and granulocyte CD66b (r:0.29). Significant associations were also found with HDLC (r:-0.38) and apoB (r:0.28; p Conclusions: This study provides evidence for a role of TGs in Leukocyte Activation, most likely depending on the composition of the TG-rich particles. These inflammatory effects may be blunted by statins. Our data contribute to the understanding of the atherogenicity of TG-rich lipoproteins.
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Coronary Leukocyte Activation in relation to progression of coronary artery disease
Frontiers of medicine, 2016Co-Authors: Marijke A. De Vries, A. Alipour, Noelle Van Der Meulen, Anho Liem, Erwin Birnie, A. Westzaan, Selvetta Van Santen, Ellen Van Der Zwan, Manuel Castro CabezasAbstract:Leukocyte Activation has been linked to atherogenesis, but there is little in vivo evidence for its role in the progression of atherosclerosis. We evaluated the predictive value for progression of coronary artery disease (CAD) of Leukocyte Activation markers in the coronary circulation. Monocyte and neutrophil CD11b, neutrophil CD66b expression and intracellular neutrophil myeloperoxidase (MPO) in the coronary arteries were determined by flow cytometry in patients undergoing coronary angiography. The primary outcome included fatal and nonfatal myocardial infarction or arterial vascular intervention due to unstable angina pectoris. In total 99 subjects who were included, 70 had CAD at inclusion (26 patients had single-vessel disease, 18 patients had twovessel disease and 26 patients had three-vessel disease). The median follow-up duration was 2242 days (interquartile range: 2142-2358). During follow-up, 13 patients (13%) developed progression of CAD. Monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO measured in blood obtained from the coronary arteries were not associated with the progression of CAD. These data indicate that coronary monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO do not predict the risk of progression of CAD.
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Glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls.
Metabolism: clinical and experimental, 2014Co-Authors: Marijke A. De Vries, B. Klop, G.-j. M. Van De Geijn, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Alipour, Noelle Van Der Meulen, Anho H. Liem, Elsbeth M. WestermanAbstract:Abstract Background Leukocyte Activation has been associated with vascular complications in type 2 diabetes mellitus (T2DM). Hyperglycemia may be involved in this Leukocyte Activation. Our aim was to investigate the role of elevated glucose concentrations on Leukocyte Activation in patients with a wide range of insulin sensitivity. Methods Leukocyte Activation was determined after ingestion of 75 gram glucose in subjects with T2DM, familial combined hyperlipidemia (FCH) and healthy controls. Leukocyte Activation markers were measured by flow cytometry. Postprandial changes were calculated as the area under the curve (AUC), and the incremental area under the curve corrected for baseline values (dAUC). Results 51 subjects (20 T2DM, 17 FCH and 14 controls) were included. Fasting neutrophil CD66b expression and CD66b-AUC were respectively 36% and 39% higher in T2DM patients than in controls (p = 0.004 and p = 0.003). Fasting neutrophil CD66b expression correlated positively with glucose-AUC (Spearman’s rho 0.481, p Conclusions These data suggest that both acute and chronic hyperglycemia, associated with insulin resistance as seen in T2DM and FCH, are involved in the increased fasting and postprandial Leukocyte Activation observed in these conditions.
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PS13 - 4. Gender differences in glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls
Nederlands Tijdschrift voor Diabetologie, 2013Co-Authors: Marijke A. De Vries, B. Klop, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Van Miltenburg, A. Alipour, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Atherosclerosis in type 2 diabetes mellitus (T2DM) and insulin resistance (IR) is characterized by a chronic inflammatory response in which Activation of Leukocytes is mandatory. Acute and chronic hyperglycemia may be involved in this Leukocyte Activation. Female T2DM patients have more severe atherosclerosis than male diabetics and differences in inflammation may be responsible for this observation.
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Leukocyte Activation by Triglyceride-Rich Lipoproteins
Arteriosclerosis thrombosis and vascular biology, 2008Co-Authors: A. Alipour, Antonie J.h.h.m. Van Oostrom, Alisa Izraeljan, C. Verseyden, Jennifer Collins, Keith N. Frayn, Thijs W.m. Plokker, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Objective— Postprandial lipemia has been linked to atherosclerosis and inflammation. Because Leukocyte Activation is obligatory for atherogenesis, Leukocyte Activation by triglyceride-rich lipoprot...
Marijke A. De Vries - One of the best experts on this subject based on the ideXlab platform.
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Abstract 17598: Inflammatory Effect of Fasting and Postprandial Triglycerides by Leukocyte Activation
Circulation, 2016Co-Authors: Benjamin Burggraaf, B. Klop, G.-j. M. Van De Geijn, A. Alipour, Marijke A. De Vries, Anho Liem, Peter De Man, Manuel Castro CabezasAbstract:Introduction: Atherosclerosis is characterized by systemic inflammation in which the Activation of Leukocytes plays a crucial role. While hypertriglyceridemia is an atherogenic condition, the underlying mechanisms have not been well defined. We aimed to evaluate the effect of triglycerides (TGs) on Leukocyte Activation. Methods: Volunteers (n=196) attended the outpatient clinic for fasting blood tests. Oral fat loading tests (n=36) were carried out to evaluate postprandial inflammation. For in vitro experiments, freshly drawn blood samples from 9 healthy volunteers were incubated with different TG emulsions: Lipoplus, Lipofundin and Intralipid and compared to LPS as positive control. Leukocyte Activation markers were measured using the flow cytometer. Results: The mean age of the total cohort was 56.7±16.5 years, 49.5% was male. Mean fasting TGs were 1.58±0.96 mmol/L. Fasting TGs were associated with monocyte CD11b (Spearman’s rho:0.29), granulocyte CD11b (r:0.30) and granulocyte CD66b (r:0.29). Significant associations were also found with HDLC (r:-0.38) and apoB (r:0.28; p Conclusions: This study provides evidence for a role of TGs in Leukocyte Activation, most likely depending on the composition of the TG-rich particles. These inflammatory effects may be blunted by statins. Our data contribute to the understanding of the atherogenicity of TG-rich lipoproteins.
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Coronary Leukocyte Activation in relation to progression of coronary artery disease
Frontiers of medicine, 2016Co-Authors: Marijke A. De Vries, A. Alipour, Noelle Van Der Meulen, Anho Liem, Erwin Birnie, A. Westzaan, Selvetta Van Santen, Ellen Van Der Zwan, Manuel Castro CabezasAbstract:Leukocyte Activation has been linked to atherogenesis, but there is little in vivo evidence for its role in the progression of atherosclerosis. We evaluated the predictive value for progression of coronary artery disease (CAD) of Leukocyte Activation markers in the coronary circulation. Monocyte and neutrophil CD11b, neutrophil CD66b expression and intracellular neutrophil myeloperoxidase (MPO) in the coronary arteries were determined by flow cytometry in patients undergoing coronary angiography. The primary outcome included fatal and nonfatal myocardial infarction or arterial vascular intervention due to unstable angina pectoris. In total 99 subjects who were included, 70 had CAD at inclusion (26 patients had single-vessel disease, 18 patients had twovessel disease and 26 patients had three-vessel disease). The median follow-up duration was 2242 days (interquartile range: 2142-2358). During follow-up, 13 patients (13%) developed progression of CAD. Monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO measured in blood obtained from the coronary arteries were not associated with the progression of CAD. These data indicate that coronary monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO do not predict the risk of progression of CAD.
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Glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls.
Metabolism: clinical and experimental, 2014Co-Authors: Marijke A. De Vries, B. Klop, G.-j. M. Van De Geijn, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Alipour, Noelle Van Der Meulen, Anho H. Liem, Elsbeth M. WestermanAbstract:Abstract Background Leukocyte Activation has been associated with vascular complications in type 2 diabetes mellitus (T2DM). Hyperglycemia may be involved in this Leukocyte Activation. Our aim was to investigate the role of elevated glucose concentrations on Leukocyte Activation in patients with a wide range of insulin sensitivity. Methods Leukocyte Activation was determined after ingestion of 75 gram glucose in subjects with T2DM, familial combined hyperlipidemia (FCH) and healthy controls. Leukocyte Activation markers were measured by flow cytometry. Postprandial changes were calculated as the area under the curve (AUC), and the incremental area under the curve corrected for baseline values (dAUC). Results 51 subjects (20 T2DM, 17 FCH and 14 controls) were included. Fasting neutrophil CD66b expression and CD66b-AUC were respectively 36% and 39% higher in T2DM patients than in controls (p = 0.004 and p = 0.003). Fasting neutrophil CD66b expression correlated positively with glucose-AUC (Spearman’s rho 0.481, p Conclusions These data suggest that both acute and chronic hyperglycemia, associated with insulin resistance as seen in T2DM and FCH, are involved in the increased fasting and postprandial Leukocyte Activation observed in these conditions.
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PS13 - 4. Gender differences in glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls
Nederlands Tijdschrift voor Diabetologie, 2013Co-Authors: Marijke A. De Vries, B. Klop, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Van Miltenburg, A. Alipour, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Atherosclerosis in type 2 diabetes mellitus (T2DM) and insulin resistance (IR) is characterized by a chronic inflammatory response in which Activation of Leukocytes is mandatory. Acute and chronic hyperglycemia may be involved in this Leukocyte Activation. Female T2DM patients have more severe atherosclerosis than male diabetics and differences in inflammation may be responsible for this observation.
Kjell Ohlsson - One of the best experts on this subject based on the ideXlab platform.
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Leukocyte Activation in atherosclerosis correlation with risk factors
Atherosclerosis, 1997Co-Authors: A M Elneihoum, P Falke, Bo Hedblad, Folke Lindgarde, Kjell OhlssonAbstract:Leukocytes have been implicated in the development of atherosclerotic vascular diseases, and numerous abnormalities of Leukocytes in conjunction with atherosclerosis have been reported. The aim of this study of middle-aged asymptomatic subjects with early atherosclerosis was to determine whether a relationship exists between the levels of plasma markers of Leukocyte Activation, i.e. cytokines and proteases and risk factors for atherosclerosis or the degree of atherosclerotic disease. Using ELISAs we measured the plasma levels of neutrophil gelatinase-associated lipocalin (NGAL), neutrophil protease 4 (NP4) as markers for neutrophil Activation, tumor necrosis factor α (TNF) and soluble TNF receptor-1 (sTNFR-1) as markers of monocyte/macrophage Activation in 156 subjects with asymptomatic carotid artery plaque detected at ultrasound examination. Plasma TNF and sTNFR-1 levels were found to correlate with systolic blood pressure (r=0.32, P<0.04 and r=0.22, P<0.05, respectively), plasma NGAL level to correlate with diastolic blood pressure (r=0.22; P<0.005), the plasma levels of sTNFR-1 and NGAL to correlate with age (r=0.28, P<0.001 and r=0.20, P<0.05, respectively). As compared with non-smokers (n=112), smokers (n=43) had higher plasma levels of TNF (2.9 vs. 1.4 μg/l; P<0.02) and of NP4 (27.5 vs. 23.4 μg/l; P<0.05). The plasma NGAL level was higher in hypertensive women (n=7) than in normotensive women (n=85) (109 vs. 87 μg/l; P<0.05). We thus demonstrated that, in subjects with asymptomatic early atherosclerosis, the plasma levels of markers of systemic Leukocyte Activation were correlated with age and blood pressure, and were higher in smokers and hypertensives. These results support the hypothesized relationship between the level of systemic Leukocyte Activation and risk factors for atherosclerotic vascular disease.
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Leukocyte Activation in atherosclerosis: correlation with risk factors
Atherosclerosis, 1997Co-Authors: A M Elneihoum, P Falke, Bo Hedblad, Folke Lindgarde, Kjell OhlssonAbstract:Leukocytes have been implicated in the development of atherosclerotic vascular diseases, and numerous abnormalities of Leukocytes in conjunction with atherosclerosis have been reported. The aim of this study of middle-aged asymptomatic subjects with early atherosclerosis was to determine whether a relationship exists between the levels of plasma markers of Leukocyte Activation, i.e. cytokines and proteases and risk factors for atherosclerosis or the degree of atherosclerotic disease. Using ELISAs we measured the plasma levels of neutrophil gelatinase-associated lipocalin (NGAL), neutrophil protease 4 (NP4) as markers for neutrophil Activation, tumor necrosis factor α (TNF) and soluble TNF receptor-1 (sTNFR-1) as markers of monocyte/macrophage Activation in 156 subjects with asymptomatic carotid artery plaque detected at ultrasound examination. Plasma TNF and sTNFR-1 levels were found to correlate with systolic blood pressure (r=0.32, P
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Leukocyte Activation Detected by Increased Plasma Levels of Inflammatory Mediators in Patients With Ischemic Cerebrovascular Diseases
Stroke, 1996Co-Authors: A M Elneihoum, P Falke, Folke Lindgarde, Lena Axelsson, E. Lundberg, Kjell OhlssonAbstract:Background and Purpose Leukocytes have been implicated in the development of ischemic atherosclerotic vascular diseases. In a prospective study we investigated whether the plasma concentrations of inflammatory mediators, ie, proteases and cytokines, as markers for systemic Leukocyte Activation, are increased in patients with acute ischemic cerebrovascular diseases. Methods Using enzyme-linked immunosorbent assays, we measured the plasma levels of neutrophil gelatinase-associated lipocalin (NGAL), neutrophil proteinase 4 (NP4), tumor necrosis factor-α (TNF), and soluble TNF receptor protein-1 p55 (sTNFR-1) in 120 patients with acute ischemic cerebrovascular insult (72 with stroke and 48 with transient ischemic attack [TIA]) and in 35 age- and sex-matched healthy subjects. Results Compared with the control group, plasma NGAL levels were higher in the stroke group (P
B. Klop - One of the best experts on this subject based on the ideXlab platform.
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Abstract 17598: Inflammatory Effect of Fasting and Postprandial Triglycerides by Leukocyte Activation
Circulation, 2016Co-Authors: Benjamin Burggraaf, B. Klop, G.-j. M. Van De Geijn, A. Alipour, Marijke A. De Vries, Anho Liem, Peter De Man, Manuel Castro CabezasAbstract:Introduction: Atherosclerosis is characterized by systemic inflammation in which the Activation of Leukocytes plays a crucial role. While hypertriglyceridemia is an atherogenic condition, the underlying mechanisms have not been well defined. We aimed to evaluate the effect of triglycerides (TGs) on Leukocyte Activation. Methods: Volunteers (n=196) attended the outpatient clinic for fasting blood tests. Oral fat loading tests (n=36) were carried out to evaluate postprandial inflammation. For in vitro experiments, freshly drawn blood samples from 9 healthy volunteers were incubated with different TG emulsions: Lipoplus, Lipofundin and Intralipid and compared to LPS as positive control. Leukocyte Activation markers were measured using the flow cytometer. Results: The mean age of the total cohort was 56.7±16.5 years, 49.5% was male. Mean fasting TGs were 1.58±0.96 mmol/L. Fasting TGs were associated with monocyte CD11b (Spearman’s rho:0.29), granulocyte CD11b (r:0.30) and granulocyte CD66b (r:0.29). Significant associations were also found with HDLC (r:-0.38) and apoB (r:0.28; p Conclusions: This study provides evidence for a role of TGs in Leukocyte Activation, most likely depending on the composition of the TG-rich particles. These inflammatory effects may be blunted by statins. Our data contribute to the understanding of the atherogenicity of TG-rich lipoproteins.
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Glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls.
Metabolism: clinical and experimental, 2014Co-Authors: Marijke A. De Vries, B. Klop, G.-j. M. Van De Geijn, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Alipour, Noelle Van Der Meulen, Anho H. Liem, Elsbeth M. WestermanAbstract:Abstract Background Leukocyte Activation has been associated with vascular complications in type 2 diabetes mellitus (T2DM). Hyperglycemia may be involved in this Leukocyte Activation. Our aim was to investigate the role of elevated glucose concentrations on Leukocyte Activation in patients with a wide range of insulin sensitivity. Methods Leukocyte Activation was determined after ingestion of 75 gram glucose in subjects with T2DM, familial combined hyperlipidemia (FCH) and healthy controls. Leukocyte Activation markers were measured by flow cytometry. Postprandial changes were calculated as the area under the curve (AUC), and the incremental area under the curve corrected for baseline values (dAUC). Results 51 subjects (20 T2DM, 17 FCH and 14 controls) were included. Fasting neutrophil CD66b expression and CD66b-AUC were respectively 36% and 39% higher in T2DM patients than in controls (p = 0.004 and p = 0.003). Fasting neutrophil CD66b expression correlated positively with glucose-AUC (Spearman’s rho 0.481, p Conclusions These data suggest that both acute and chronic hyperglycemia, associated with insulin resistance as seen in T2DM and FCH, are involved in the increased fasting and postprandial Leukocyte Activation observed in these conditions.
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Vitamin D3 mediated effects on postprandial Leukocyte Activation and arterial stiffness in men and women
European journal of clinical nutrition, 2014Co-Authors: B. Klop, G.-j. M. Van De Geijn, T. L. Njo, Hans Janssen, J.w.f. Elte, Erwin Birnie, Hans Jansen, J W Jukema, M. Castro CabezasAbstract:Postprandial inflammation is considered to be pro-atherogenic. Vitamin D can reduce inflammation and arterial stiffness. We hypothesized that vitamin D3 improves postprandial arterial elasticity by the modulation of Leukocyte Activation. Healthy volunteers underwent two oral fat-loading tests (OFLTs). The augmentation index (AIx) and flow cytometric quantification of Leukocyte Activation markers were measured. After the first OFLT, 100 000 IU of vitamin D3 was administered and a second OFLT was carried out 7 days later. Six men and six women were included. A favorable reduction in AIx was found after vitamin D3 supplementation (P=0.042) in both genders. After vitamin D3, exclusively in women a reduction in the area under the postprandial curve for monocytes CD11b and CD35 by 10.5% (P=0.016) and 12.5% (P=0.04) and neutrophil CD11b by 17.0% (P=0.014) was observed. In conclusion, vitamin D3 probably increased postprandial arterial elasticity in men and women, but reduced postprandial Leukocyte Activation exclusively in women.
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Leukocyte cell population data (volume conductivity scatter) in postprandial Leukocyte Activation.
International Journal of Laboratory Hematology, 2013Co-Authors: B. Klop, G.-j. M. Van De Geijn, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Van Miltenburg, Laura Fernández-sender, J.w.f. Elte, M. Castro CabezasAbstract:Summary Introduction Changes in Leukocyte cell population data have been reported in various infectious diseases, but little is known in other inflammatory conditions such as the postprandial state. We investigated whether Leukocyte cell population data change during postprandial Leukocyte Activation. Methods Healthy volunteers underwent a standardized oral fat loading test (OFLT). Flowcytometric quantitation of Leukocyte Activation markers CD11b, CD66b, CD35, and CD36, together with Leukocyte cell population data from LH750 hematology analyzers were measured fasting and at 4 and 8 h postprandially. Results Twelve volunteers were included. Postprandial Leukocyte Activation was confirmed by increased expression of CD11b by monocytes (+11.7%) and neutrophils (+15.0%) and by increased expression of CD66b (+14.7%) and CD35 (+16.6%) by neutrophils at T = 4 h. The mean scatter from neutrophils, reflecting granularity, significantly decreased at T = 4 h (P
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PS13 - 4. Gender differences in glucose-dependent Leukocyte Activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls
Nederlands Tijdschrift voor Diabetologie, 2013Co-Authors: Marijke A. De Vries, B. Klop, T. L. Njo, Hans Janssen, Arie P. Rietveld, A. Van Miltenburg, A. Alipour, Jan Willem F. Elte, Manuel Castro CabezasAbstract:Atherosclerosis in type 2 diabetes mellitus (T2DM) and insulin resistance (IR) is characterized by a chronic inflammatory response in which Activation of Leukocytes is mandatory. Acute and chronic hyperglycemia may be involved in this Leukocyte Activation. Female T2DM patients have more severe atherosclerosis than male diabetics and differences in inflammation may be responsible for this observation.