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Lo R Presti - One of the best experts on this subject based on the ideXlab platform.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca 2 content in young adults with acute myocardial infarction evaluation at the initial stage and after 12 months
Clinical Hemorheology and Microcirculation, 2004Co-Authors: G Caimi, Baldassare Canino, M Montana, E Hoffmann, F Dispensa, Egle Incalcaterra, Maria Flavia Casciolo, A Catania, Lo R PrestiAbstract:Our aim was to examine two aspects of polymorphonuclear Leukocyte (PMN) rheology (Membrane fluidity and cytosolic Ca 2 + content), at baseline and after in vitro activation, in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after 12 months. We enrolled 21 AMI subjects aged ≤ 45 years (mean age 41.1 ′ 3.5 years) and evaluated PMN Membrane fluidity, labelling intact PMN cells with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene and the PMN cytosolic Ca 2 + content marking PMN cells with the fluorescent probe Fura 2-AM, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). During the initial stage PMN Membrane fluidity and cytosolic Ca 2 + content did not distinguish AMI patients from control subjects; after 12 months, when compared with the initial stage, PMN cytosolic Ca 2 + content was significantly increased. In vitro PMN activation with PMA and fMLP caused no variation of the two PMN parameters in control subjects, while in AMI patients Membrane fluidity decreased and cytosolic Ca 2 + content increased; the same behaviour pattern was observed after 12 months. The constant functional alteration of PMN cells in young AMI patients highlights the role of activated Leukocytes as a component of the inflammatory reaction that follows ischemia.
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acute ischemic stroke polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration at baseline and after chemotactic activation
Stroke, 2000Co-Authors: G Caimi, Baldassare Canino, M Montana, F Ferrara, Francesco Meli, Caterina Carollo, Lo R PrestiAbstract:Background and Purpose —Several reports have considered the role of systemic Leukocytes in acute ischemic stroke (AIS). Initially, greater attention was focused on the Leukocyte count and subsequently on their adhesiveness, aggregation, rheology, and activation. The aim of this study was the evaluation of certain polymorphonuclear Leukocyte (PMN) parameters, reflecting their rheology and activation, in subjects with AIS. Methods —In a group of 19 subjects with AIS and in a control group of 18 subjects with asymptomatic vascular atherosclerotic disease, we evaluated the PMN Membrane fluidity and cytosolic Ca2+ concentration at baseline and after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and N -formyl-methionyl-leucyl-phenylalanine (fMLP). Results —From the obtained data, it is evident that at baseline only PMN Membrane fluidity distinguishes control subjects from AIS subjects. After PMN activation with PMA and fMLP, prolonged for 5 and 15 minutes, we found an increase in PMN cytosolic Ca2+ concentration and a decrease in PMN Membrane fluidity only in subjects with AIS. Conclusions —These findings emphasize that in subjects with AIS a functional alteration of systemic PMN cells is clearly expressed during chemotactic activation, although the mechanism of this abnormality is not yet explained.
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polymorphonuclear Leukocyte Membrane fluidity before and after activation in subjects with insulin resistance
Acta Diabetologica, 2000Co-Authors: G Caimi, Baldassare Canino, D Sinagra, A M Scarpitta, M Montana, V Bonaventura, Lo R PrestiAbstract:The aim of this research was the evaluation of polymorphonuclear Leukocyte (PMN) Membrane fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma Membrane fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN Membrane fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethyl-amino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMN) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN memebrane fluidity in subjects wit insulin resistance. After PMN activation with PMA and fMLP, no significant variation in Membrane fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN Membrane fluidity was found only after activation with fMLP. The behavior of PMN Membrane fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration in diabetes mellitus
Acta Diabetologica, 1998Co-Authors: G Caimi, Baldassare Canino, M Montana, G Ventimiglia, A Catania, Lo R PrestiAbstract:We evaluated polymorphonuclear Membrane (PMN) fluidity in 32 subjects with type 1 diabetes mellitus, 38 subjects with type 2 diabetes mellitus and 38 normal control subjects, by marking intact and unstimulated PMN cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). We also evaluated PMN cytosolic Ca2+ content by marking intact and unstimulated PMN cells with the fluorescent probe Fura 2-AM. PMN Membrane fluidity differentiated normal subjects from type 1 and 2 diabetic subjects. The PMN cytosolic Ca2+ concentration did not discriminate type 1 and 2 diabetic subjects from normal control subjects. No statistical correlation was found between PMN Membrane fluidity and PMN cytosolic Ca2+ concentration in any of the groups of subjects, nor were significant correlations found between PMN Membrane fluidity and cytosolic Ca2+ concentration in several plasma parameters (serum glucose, cholesterol and triglycerides). In conclusion, in type 1 and 2 diabetic patients we found a decrease in PMN Membrane fluidity and this decrease, which was greater in type 2 diabetic patients, may be a marker of PMN dysfunction.
G Caimi - One of the best experts on this subject based on the ideXlab platform.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca 2 content in young adults with acute myocardial infarction evaluation at the initial stage and after 12 months
Clinical Hemorheology and Microcirculation, 2004Co-Authors: G Caimi, Baldassare Canino, M Montana, E Hoffmann, F Dispensa, Egle Incalcaterra, Maria Flavia Casciolo, A Catania, Lo R PrestiAbstract:Our aim was to examine two aspects of polymorphonuclear Leukocyte (PMN) rheology (Membrane fluidity and cytosolic Ca 2 + content), at baseline and after in vitro activation, in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after 12 months. We enrolled 21 AMI subjects aged ≤ 45 years (mean age 41.1 ′ 3.5 years) and evaluated PMN Membrane fluidity, labelling intact PMN cells with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene and the PMN cytosolic Ca 2 + content marking PMN cells with the fluorescent probe Fura 2-AM, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). During the initial stage PMN Membrane fluidity and cytosolic Ca 2 + content did not distinguish AMI patients from control subjects; after 12 months, when compared with the initial stage, PMN cytosolic Ca 2 + content was significantly increased. In vitro PMN activation with PMA and fMLP caused no variation of the two PMN parameters in control subjects, while in AMI patients Membrane fluidity decreased and cytosolic Ca 2 + content increased; the same behaviour pattern was observed after 12 months. The constant functional alteration of PMN cells in young AMI patients highlights the role of activated Leukocytes as a component of the inflammatory reaction that follows ischemia.
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acute ischemic stroke polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration at baseline and after chemotactic activation
Stroke, 2000Co-Authors: G Caimi, Baldassare Canino, M Montana, F Ferrara, Francesco Meli, Caterina Carollo, Lo R PrestiAbstract:Background and Purpose —Several reports have considered the role of systemic Leukocytes in acute ischemic stroke (AIS). Initially, greater attention was focused on the Leukocyte count and subsequently on their adhesiveness, aggregation, rheology, and activation. The aim of this study was the evaluation of certain polymorphonuclear Leukocyte (PMN) parameters, reflecting their rheology and activation, in subjects with AIS. Methods —In a group of 19 subjects with AIS and in a control group of 18 subjects with asymptomatic vascular atherosclerotic disease, we evaluated the PMN Membrane fluidity and cytosolic Ca2+ concentration at baseline and after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and N -formyl-methionyl-leucyl-phenylalanine (fMLP). Results —From the obtained data, it is evident that at baseline only PMN Membrane fluidity distinguishes control subjects from AIS subjects. After PMN activation with PMA and fMLP, prolonged for 5 and 15 minutes, we found an increase in PMN cytosolic Ca2+ concentration and a decrease in PMN Membrane fluidity only in subjects with AIS. Conclusions —These findings emphasize that in subjects with AIS a functional alteration of systemic PMN cells is clearly expressed during chemotactic activation, although the mechanism of this abnormality is not yet explained.
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polymorphonuclear Leukocyte Membrane fluidity before and after activation in subjects with insulin resistance
Acta Diabetologica, 2000Co-Authors: G Caimi, Baldassare Canino, D Sinagra, A M Scarpitta, M Montana, V Bonaventura, Lo R PrestiAbstract:The aim of this research was the evaluation of polymorphonuclear Leukocyte (PMN) Membrane fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma Membrane fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN Membrane fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethyl-amino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMN) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN memebrane fluidity in subjects wit insulin resistance. After PMN activation with PMA and fMLP, no significant variation in Membrane fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN Membrane fluidity was found only after activation with fMLP. The behavior of PMN Membrane fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration in diabetes mellitus
Acta Diabetologica, 1998Co-Authors: G Caimi, Baldassare Canino, M Montana, G Ventimiglia, A Catania, Lo R PrestiAbstract:We evaluated polymorphonuclear Membrane (PMN) fluidity in 32 subjects with type 1 diabetes mellitus, 38 subjects with type 2 diabetes mellitus and 38 normal control subjects, by marking intact and unstimulated PMN cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). We also evaluated PMN cytosolic Ca2+ content by marking intact and unstimulated PMN cells with the fluorescent probe Fura 2-AM. PMN Membrane fluidity differentiated normal subjects from type 1 and 2 diabetic subjects. The PMN cytosolic Ca2+ concentration did not discriminate type 1 and 2 diabetic subjects from normal control subjects. No statistical correlation was found between PMN Membrane fluidity and PMN cytosolic Ca2+ concentration in any of the groups of subjects, nor were significant correlations found between PMN Membrane fluidity and cytosolic Ca2+ concentration in several plasma parameters (serum glucose, cholesterol and triglycerides). In conclusion, in type 1 and 2 diabetic patients we found a decrease in PMN Membrane fluidity and this decrease, which was greater in type 2 diabetic patients, may be a marker of PMN dysfunction.
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erythrocyte platelet and polymorphonuclear Leukocyte Membrane dynamic properties in essential hypertension
Clinical Hemorheology and Microcirculation, 1997Co-Authors: G CaimiAbstract:In subjects with essential hypertension we evaluated, respectively, the red cell Membrane protein lateral mobility (obtained marking intact red blood cells with pyrene-3-maleimide (3-PM)), the erythrocyte Membrane fluidity (obtained marking intact erythrocytes with 10-(1-pyrene) decanoic acid), the red cell Membrane transverse fluidity gradient (ob- tained marking intact red blood cells with a set of fatty acid fluorescent probes (2-AP, 6-AS, 9-AS, 12-AS)), the platelet Membrane fluidity (obtained marking intact and unstimulated platelets with 1,6-diphenyl-1,3,5-hexatriene (DPH) and with 1-(4-(trimethylamino)phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH)) and the polymorphonuclear Membrane fluidity (ob- tained marking intact and unstimulated polymorphonuclear cells with TMA-DPH). From the obtained data it is evident that: (1) red cell Membrane protein lateral mobility does not distinguish normals from hypertensives; (2) erythrocyte Membrane fluidity and red cell Membrane transverse fluidity gradient clearly discriminate normals from hypertensives; (3) platelet mem- brane fluidity differentiates normals from hypertensives only when DPH is used as fluorescent probe; (4) polymorphonuclear Membrane fluidity does not distinguish normals from hypertensives. Our results show that in essential hypertension a different behaviour of the Membrane dynamic properties in the circulating blood cells is evident.
Baldassare Canino - One of the best experts on this subject based on the ideXlab platform.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca 2 content in young adults with acute myocardial infarction evaluation at the initial stage and after 12 months
Clinical Hemorheology and Microcirculation, 2004Co-Authors: G Caimi, Baldassare Canino, M Montana, E Hoffmann, F Dispensa, Egle Incalcaterra, Maria Flavia Casciolo, A Catania, Lo R PrestiAbstract:Our aim was to examine two aspects of polymorphonuclear Leukocyte (PMN) rheology (Membrane fluidity and cytosolic Ca 2 + content), at baseline and after in vitro activation, in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after 12 months. We enrolled 21 AMI subjects aged ≤ 45 years (mean age 41.1 ′ 3.5 years) and evaluated PMN Membrane fluidity, labelling intact PMN cells with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene and the PMN cytosolic Ca 2 + content marking PMN cells with the fluorescent probe Fura 2-AM, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). During the initial stage PMN Membrane fluidity and cytosolic Ca 2 + content did not distinguish AMI patients from control subjects; after 12 months, when compared with the initial stage, PMN cytosolic Ca 2 + content was significantly increased. In vitro PMN activation with PMA and fMLP caused no variation of the two PMN parameters in control subjects, while in AMI patients Membrane fluidity decreased and cytosolic Ca 2 + content increased; the same behaviour pattern was observed after 12 months. The constant functional alteration of PMN cells in young AMI patients highlights the role of activated Leukocytes as a component of the inflammatory reaction that follows ischemia.
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acute ischemic stroke polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration at baseline and after chemotactic activation
Stroke, 2000Co-Authors: G Caimi, Baldassare Canino, M Montana, F Ferrara, Francesco Meli, Caterina Carollo, Lo R PrestiAbstract:Background and Purpose —Several reports have considered the role of systemic Leukocytes in acute ischemic stroke (AIS). Initially, greater attention was focused on the Leukocyte count and subsequently on their adhesiveness, aggregation, rheology, and activation. The aim of this study was the evaluation of certain polymorphonuclear Leukocyte (PMN) parameters, reflecting their rheology and activation, in subjects with AIS. Methods —In a group of 19 subjects with AIS and in a control group of 18 subjects with asymptomatic vascular atherosclerotic disease, we evaluated the PMN Membrane fluidity and cytosolic Ca2+ concentration at baseline and after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and N -formyl-methionyl-leucyl-phenylalanine (fMLP). Results —From the obtained data, it is evident that at baseline only PMN Membrane fluidity distinguishes control subjects from AIS subjects. After PMN activation with PMA and fMLP, prolonged for 5 and 15 minutes, we found an increase in PMN cytosolic Ca2+ concentration and a decrease in PMN Membrane fluidity only in subjects with AIS. Conclusions —These findings emphasize that in subjects with AIS a functional alteration of systemic PMN cells is clearly expressed during chemotactic activation, although the mechanism of this abnormality is not yet explained.
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polymorphonuclear Leukocyte Membrane fluidity before and after activation in subjects with insulin resistance
Acta Diabetologica, 2000Co-Authors: G Caimi, Baldassare Canino, D Sinagra, A M Scarpitta, M Montana, V Bonaventura, Lo R PrestiAbstract:The aim of this research was the evaluation of polymorphonuclear Leukocyte (PMN) Membrane fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma Membrane fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN Membrane fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethyl-amino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMN) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN memebrane fluidity in subjects wit insulin resistance. After PMN activation with PMA and fMLP, no significant variation in Membrane fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN Membrane fluidity was found only after activation with fMLP. The behavior of PMN Membrane fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.
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polymorphonuclear Leukocyte Membrane fluidity and cytosolic ca2 concentration in diabetes mellitus
Acta Diabetologica, 1998Co-Authors: G Caimi, Baldassare Canino, M Montana, G Ventimiglia, A Catania, Lo R PrestiAbstract:We evaluated polymorphonuclear Membrane (PMN) fluidity in 32 subjects with type 1 diabetes mellitus, 38 subjects with type 2 diabetes mellitus and 38 normal control subjects, by marking intact and unstimulated PMN cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). We also evaluated PMN cytosolic Ca2+ content by marking intact and unstimulated PMN cells with the fluorescent probe Fura 2-AM. PMN Membrane fluidity differentiated normal subjects from type 1 and 2 diabetic subjects. The PMN cytosolic Ca2+ concentration did not discriminate type 1 and 2 diabetic subjects from normal control subjects. No statistical correlation was found between PMN Membrane fluidity and PMN cytosolic Ca2+ concentration in any of the groups of subjects, nor were significant correlations found between PMN Membrane fluidity and cytosolic Ca2+ concentration in several plasma parameters (serum glucose, cholesterol and triglycerides). In conclusion, in type 1 and 2 diabetic patients we found a decrease in PMN Membrane fluidity and this decrease, which was greater in type 2 diabetic patients, may be a marker of PMN dysfunction.
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Polymorphonuclear Leukocyte Membrane fluidity and cytosolic Ca2+ content in different clinical conditions.
Clinical Hemorheology and Microcirculation, 1997Co-Authors: Gregorio Caimi, Baldassare Canino, M Montana, G Ventimiglia, A Catania, Rosalia Lo PrestiAbstract:The aim of the study was to evaluate the polymorphonuclear Leukocyte (PMN) Membrane fluidity and PMN cytosolic Ca 2+ content in several clinical conditions: diabetes mellitus, vascular atherosclerotic disease (VAD), chronic renal failure (CRF), essential hypertension (EH). In 13 subjects with insulin-dependent diabetes mellitus (IDDM), in 24 subjects with non-insulin-dependent diabetes mellitus (NIDDM), in 42 VAD subjects, in 23 VAD subjects with NIDDM, in 15 subjects with CRF and in 12 subjects with EH, we determined the PMN Membrane fluidity, obtained marking unstimulated PMN cells with fluorescent probe 1-(4-(trimethylamino)phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH), and considering the fluorescence polarization degree, and the PMN cytosolic Ca 2+ content, obtained marking unstimulated PMN cells with the fluorescent probe Fura2-AM and considering the ratio between the Fura2-Ca 2+ complex and the unchelated Fura2 fluorescence intensity. From the obtained data it is evident that PMN Membrane fluidity does not distinguish normals from IDDM subjects, NIDDM subjects, VAD subjects with and without NIDDM, CRF subjects and hypertensives. PMN cytosolic Ca 2+ content, in comparison with normal controls, is significantly increased in VAD subjects ( p< 0:01), in VAD subjects with NIDDM ( p< 0:001), in CRF subjects ( p< 0:001) and in hypertensives ( p< 0:05). No correlation was found between PMN Membrane fluidity and PMN cytosolic Ca 2+ content. The study of these PMN parameters can be useful in the understanding of the role of Leukocytes in the vascular damage that characterizes these clinical conditions.
Uma Kumar - One of the best experts on this subject based on the ideXlab platform.
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expression and significance of Leukocyte Membrane cofactor protein transcript in systemic lupus erythematosus
Lupus, 2012Co-Authors: Bintili Biswas, Uma KumarAbstract:Membrane cofactor protein (MCP) is a complement regulatory protein ubiquitously expressed on most nucleated cells. Since MCP protects autologous cells from complement-mediated injury, it is suggested to have a protective role against the self-tissue damage in inflammatory conditions such as systemic lupus erythematosus (SLE). However, the relevance of MCP in human SLE is not well explored. To assess the significance of MCP in SLE, we studied expression of Leukocyte MCP transcript in 60 healthy individuals (controls) and 60 patients with SLE and correlated that with the levels of circulating immune complex (CIC), C3, C3d and SLEDAI scores. The levels of Leukocyte MCP transcript were significantly higher (p < 0.001) in patients with SLE than the controls. Furthermore, MCP transcript levels exhibited significant positive correlations with SLEDAI scores and CIC level and a negative correlation with C3d level in patients. Twelve patients were followed-up until remission. The levels of MCP transcripts decreased significantly during remission as compared with the state of active disease. These findings suggest that in SLE, the expression of Leukocyte MCP at the mRNA level is closely related to disease activity. A protective role of MCP in response to increased disease burden may be speculated. The follow-up study suggested MCP as a potential disease marker.
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Expression and significance of Leukocyte Membrane cofactor protein transcript in systemic lupus erythematosus
Lupus, 2012Co-Authors: Bintili Biswas, Uma KumarAbstract:Membrane cofactor protein (MCP) is a complement regulatory protein ubiquitously expressed on most nucleated cells. Since MCP protects autologous cells from complement-mediated injury, it is suggested to have a protective role against the self-tissue damage in inflammatory conditions such as systemic lupus erythematosus (SLE). However, the relevance of MCP in human SLE is not well explored. To assess the significance of MCP in SLE, we studied expression of Leukocyte MCP transcript in 60 healthy individuals (controls) and 60 patients with SLE and correlated that with the levels of circulating immune complex (CIC), C3, C3d and SLEDAI scores. The levels of Leukocyte MCP transcript were significantly higher (p
Jan Palmblad - One of the best experts on this subject based on the ideXlab platform.
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in vitro effects of ethanol on polymorphonuclear Leukocyte Membrane receptor expression and mobility
Biochemical Pharmacology, 1996Co-Authors: Eva Nilsson, Gunilla Hallden, Karleric Magnusson, Jan PalmbladAbstract:The hampered inflammation and host defense seen in alcoholics may be due to impairment of functional responses of neutrophil polymorphonuclear Leukocytes (PMN). We have shown that ethanol inhibits the oxidative metabolism of PMN induced by surface receptor dependent stimuli, such as N-formyl-methionyl-leucyl-phenylalanine (fMLP) and opsonized zymosan. Because the unresponsiveness might be due to reduced numbers of surface receptors, we assessed the expression of CR1, Fc-γ, and fMLP receptors as well as Membrane fluidity after treatment of PMN with ethanol in vitro. Ethanol impaired the induced expression of CR1 and fMLP receptors to 71% and 51% of control, respectively, but did not affect the resting level of CR1 nor Fc-γ receptor expression. Furthermore, the mobility of cell Membrane glycoconjugates was increased by ethanol. However, phagocytosis, a functional response dependent on Membrane rheology, was unaffected. Because the results indicated an effect of ethanol on mobilization of receptors from intracellular stores, we assessed lactoferrin release, which was reduced to 59%. Thus, ethanol appeared to hamper the upregulation of PMN surface receptors or functional subsets of those stored in granules. Ethanol also increased the mobility of the cell Membrane. These reactions were accompanied by reductions in the functional responses mediated by either class of receptors.