The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Rutger J Ploeg - One of the best experts on this subject based on the ideXlab platform.
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relationship between duration of brain death and hemodynamic in stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney International, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Gert J Ter Horst, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Rutger J PloegAbstract:Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys. Background Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death–induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. Methods In Wistar rats, short-term (1hour) or long-term (6hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1hour and 6hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Results Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Conclusion Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney international, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Gert J. Ter Horst, Rutger J PloegAbstract:Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Effects of Brain Death and Hemodynamic Status on Function and Immunologic Activation of the Potential Donor Liver in the Rat
Annals of surgery, 2000Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Gert J. Ter Horst, Paul De Vos, Armand R. J. Girbes, Folkert Postema, Rutger J PloegAbstract:Liver transplantation has evolved from an experimental operation in the 1970s to a standard treatment for end-stage liver disease today. There have been many achievements in organ transplantation in recent years, but major problems on the donor side remain, the shortage of donors being one. The lack of suitable donor organs and the increasing number of patients requiring an organ graft have resulted in the frequent acceptance of less-than-optimal donor livers for transplantation. These so-called marginal donor livers have a greater risk of primary dysfunction than livers retrieved from so-called optimal donors. Organs with primary dysfunction have a significantly lower graft survival, 1,2 more acute rejection episodes, and a greater likelihood of developing chronic transplant dysfunction than organs with initially good function. 3–5 Primary dysfunction is associated with significant complications, an increased retransplantation rate, and death. Primary dysfunction can be caused by several factors, among which ischemia and reperfusion injury are of major importance. During the past few years, several groups have focused on the nonphysiologic state of brain death before organ retrieval as another potential risk factor for the outcome after transplantation. 6–8 Brain death has been shown to have definite effects on hemodynamic stability, 9,10 hormone regulation, 11,12 and the inflammatory reactivity of the heart. 13,14 Only scarce information is available, however, on the relation between brain death and organs such as the donor liver. 6,7,15 For this study, we developed a brain-death model in the rat that mimics either optimal (normotensive) or marginal (hypotensive) brain-dead donors. The model correlates well with the injury seen in human donors, where hemodynamic instability is inevitably encountered during the state of brain death unless appropriately treated. With this rat model, we investigated the effects of brain death in normotensive and hypotensive donors. We studied the effects of brain death on the function and the inflammatory status of donor livers. Subsequently, we compared the quality of livers obtained from control rats with those of normotensive and hypotensive brain-dead rats, after short or long intervals after induction of brain death.
Naomi W. Lucchi - One of the best experts on this subject based on the ideXlab platform.
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Immunologic Activation of human syncytiotrophoblast by Plasmodium falciparum.
Malaria journal, 2008Co-Authors: Naomi W. Lucchi, David S. Peterson, Julie M. MooreAbstract:Malaria during pregnancy is characterized by the sequestration of malaria-infected red blood cells (iRBC) in the intervillous spaces of the placenta, often accompanied by the infiltration of maternal mononuclear cells, causing substantial maternal and foetal/infant morbidity. The iRBC bind to receptors expressed by the syncytiotrophoblast (ST). How ST responds to this interaction remains poorly understood. Because it is known that ST is immunoactive and can respond to infectious agents, the consequences of this ST-iRBC interaction should be investigated. An in vitro system was used to assess the biochemical and Immunological changes induced in ST by ST-adherent iRBCs. Changes in ST mitogen-activated protein kinase (MAPK) Activation were assessed by immunoblotting and mRNA expression levels of selected cytokine and chemokines in primary ST bound by iRBC were determined using real-time, reverse transcription PCR. In addition, secreted cytokine and chemokine proteins were assayed by standard ELISA, and chemotaxis of PBMC was assessed using a two-chamber assay system. Following iRBC/ST interaction, ST C-Jun N-terminal kinase 1 (JNK1) was activated and modest increases in the mRNA expression of TGF-beta and IL-8/CXCL8 were observed. In addition, this interaction increased secretion of MIF and MIP-1alpha/CCL3 by ST and induced migration of PBMC towards iRBC-stimulated ST. Results from this study provide the first evidence that ST participates in shaping the local Immunological milieu and in the recruitment of maternal immune cells to the maternal blood space during placental malaria infection.
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Immunologic Activation of human syncytiotrophoblast by plasmodium falciparum
Malaria Journal, 2008Co-Authors: Naomi W. Lucchi, David S. Peterson, Julie M. MooreAbstract:Background Malaria during pregnancy is characterized by the sequestration of malaria-infected red blood cells (iRBC) in the intervillous spaces of the placenta, often accompanied by the infiltration of maternal mononuclear cells, causing substantial maternal and foetal/infant morbidity. The iRBC bind to receptors expressed by the syncytiotrophoblast (ST). How ST responds to this interaction remains poorly understood. Because it is known that ST is immunoactive and can respond to infectious agents, the consequences of this ST-iRBC interaction should be investigated.
Julie M. Moore - One of the best experts on this subject based on the ideXlab platform.
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Immunologic Activation of human syncytiotrophoblast by Plasmodium falciparum.
Malaria journal, 2008Co-Authors: Naomi W. Lucchi, David S. Peterson, Julie M. MooreAbstract:Malaria during pregnancy is characterized by the sequestration of malaria-infected red blood cells (iRBC) in the intervillous spaces of the placenta, often accompanied by the infiltration of maternal mononuclear cells, causing substantial maternal and foetal/infant morbidity. The iRBC bind to receptors expressed by the syncytiotrophoblast (ST). How ST responds to this interaction remains poorly understood. Because it is known that ST is immunoactive and can respond to infectious agents, the consequences of this ST-iRBC interaction should be investigated. An in vitro system was used to assess the biochemical and Immunological changes induced in ST by ST-adherent iRBCs. Changes in ST mitogen-activated protein kinase (MAPK) Activation were assessed by immunoblotting and mRNA expression levels of selected cytokine and chemokines in primary ST bound by iRBC were determined using real-time, reverse transcription PCR. In addition, secreted cytokine and chemokine proteins were assayed by standard ELISA, and chemotaxis of PBMC was assessed using a two-chamber assay system. Following iRBC/ST interaction, ST C-Jun N-terminal kinase 1 (JNK1) was activated and modest increases in the mRNA expression of TGF-beta and IL-8/CXCL8 were observed. In addition, this interaction increased secretion of MIF and MIP-1alpha/CCL3 by ST and induced migration of PBMC towards iRBC-stimulated ST. Results from this study provide the first evidence that ST participates in shaping the local Immunological milieu and in the recruitment of maternal immune cells to the maternal blood space during placental malaria infection.
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Immunologic Activation of human syncytiotrophoblast by plasmodium falciparum
Malaria Journal, 2008Co-Authors: Naomi W. Lucchi, David S. Peterson, Julie M. MooreAbstract:Background Malaria during pregnancy is characterized by the sequestration of malaria-infected red blood cells (iRBC) in the intervillous spaces of the placenta, often accompanied by the infiltration of maternal mononuclear cells, causing substantial maternal and foetal/infant morbidity. The iRBC bind to receptors expressed by the syncytiotrophoblast (ST). How ST responds to this interaction remains poorly understood. Because it is known that ST is immunoactive and can respond to infectious agents, the consequences of this ST-iRBC interaction should be investigated.
Joost A B Van Der Hoeven - One of the best experts on this subject based on the ideXlab platform.
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relationship between duration of brain death and hemodynamic in stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney International, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Gert J Ter Horst, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Rutger J PloegAbstract:Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys. Background Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death–induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. Methods In Wistar rats, short-term (1hour) or long-term (6hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1hour and 6hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Results Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Conclusion Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney international, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Gert J. Ter Horst, Rutger J PloegAbstract:Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Effects of Brain Death and Hemodynamic Status on Function and Immunologic Activation of the Potential Donor Liver in the Rat
Annals of surgery, 2000Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Gert J. Ter Horst, Paul De Vos, Armand R. J. Girbes, Folkert Postema, Rutger J PloegAbstract:Liver transplantation has evolved from an experimental operation in the 1970s to a standard treatment for end-stage liver disease today. There have been many achievements in organ transplantation in recent years, but major problems on the donor side remain, the shortage of donors being one. The lack of suitable donor organs and the increasing number of patients requiring an organ graft have resulted in the frequent acceptance of less-than-optimal donor livers for transplantation. These so-called marginal donor livers have a greater risk of primary dysfunction than livers retrieved from so-called optimal donors. Organs with primary dysfunction have a significantly lower graft survival, 1,2 more acute rejection episodes, and a greater likelihood of developing chronic transplant dysfunction than organs with initially good function. 3–5 Primary dysfunction is associated with significant complications, an increased retransplantation rate, and death. Primary dysfunction can be caused by several factors, among which ischemia and reperfusion injury are of major importance. During the past few years, several groups have focused on the nonphysiologic state of brain death before organ retrieval as another potential risk factor for the outcome after transplantation. 6–8 Brain death has been shown to have definite effects on hemodynamic stability, 9,10 hormone regulation, 11,12 and the inflammatory reactivity of the heart. 13,14 Only scarce information is available, however, on the relation between brain death and organs such as the donor liver. 6,7,15 For this study, we developed a brain-death model in the rat that mimics either optimal (normotensive) or marginal (hypotensive) brain-dead donors. The model correlates well with the injury seen in human donors, where hemodynamic instability is inevitably encountered during the state of brain death unless appropriately treated. With this rat model, we investigated the effects of brain death in normotensive and hypotensive donors. We studied the effects of brain death on the function and the inflammatory status of donor livers. Subsequently, we compared the quality of livers obtained from control rats with those of normotensive and hypotensive brain-dead rats, after short or long intervals after induction of brain death.
Reni L Freund - One of the best experts on this subject based on the ideXlab platform.
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relationship between duration of brain death and hemodynamic in stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney International, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Gert J Ter Horst, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Rutger J PloegAbstract:Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys. Background Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death–induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. Methods In Wistar rats, short-term (1hour) or long-term (6hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1hour and 6hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Results Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Conclusion Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased Immunologic Activation of donor kidneys
Kidney international, 2003Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Henri G D Leuvenink, Gert J. Ter Horst, Rutger J PloegAbstract:Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the Immunologic status of the kidney. Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory Activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune Activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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Effects of Brain Death and Hemodynamic Status on Function and Immunologic Activation of the Potential Donor Liver in the Rat
Annals of surgery, 2000Co-Authors: Joost A B Van Der Hoeven, Grietje Molema, Reni L Freund, Janneke Wiersema, Reinout Van Schilfgaarde, Gert J. Ter Horst, Paul De Vos, Armand R. J. Girbes, Folkert Postema, Rutger J PloegAbstract:Liver transplantation has evolved from an experimental operation in the 1970s to a standard treatment for end-stage liver disease today. There have been many achievements in organ transplantation in recent years, but major problems on the donor side remain, the shortage of donors being one. The lack of suitable donor organs and the increasing number of patients requiring an organ graft have resulted in the frequent acceptance of less-than-optimal donor livers for transplantation. These so-called marginal donor livers have a greater risk of primary dysfunction than livers retrieved from so-called optimal donors. Organs with primary dysfunction have a significantly lower graft survival, 1,2 more acute rejection episodes, and a greater likelihood of developing chronic transplant dysfunction than organs with initially good function. 3–5 Primary dysfunction is associated with significant complications, an increased retransplantation rate, and death. Primary dysfunction can be caused by several factors, among which ischemia and reperfusion injury are of major importance. During the past few years, several groups have focused on the nonphysiologic state of brain death before organ retrieval as another potential risk factor for the outcome after transplantation. 6–8 Brain death has been shown to have definite effects on hemodynamic stability, 9,10 hormone regulation, 11,12 and the inflammatory reactivity of the heart. 13,14 Only scarce information is available, however, on the relation between brain death and organs such as the donor liver. 6,7,15 For this study, we developed a brain-death model in the rat that mimics either optimal (normotensive) or marginal (hypotensive) brain-dead donors. The model correlates well with the injury seen in human donors, where hemodynamic instability is inevitably encountered during the state of brain death unless appropriately treated. With this rat model, we investigated the effects of brain death in normotensive and hypotensive donors. We studied the effects of brain death on the function and the inflammatory status of donor livers. Subsequently, we compared the quality of livers obtained from control rats with those of normotensive and hypotensive brain-dead rats, after short or long intervals after induction of brain death.