czs – -Translation – Keybot Dictionary

Spacer TTN Translation Network TTN TTN Login Deutsch Français Spacer Help
Source Languages Target Languages
Keybot 13 Results  www.uantwerpen.be
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Multiple sclerose (MS) is een chronische inflammatoire auto-immuunaandoening van het centrale zenuwstelsel (CZS). Deze neurodegeneratieve ziekte wordt gekenmerkt door multifocale inflammatie, demyelinatie, axonale degeneratie en astrogliosis.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Multiple sclerosis (MS) is the leading cause of non-traumatic disability in young adults. Although growing insights into disease mechanisms underlying MS have resulted in the development of new therapeutic strategies, none of the currently available treatments results in permanent stabilization or cure of MS. Current research efforts are focused on further unraveling MS immunopathogenesis as well as on finding ways to specifically manipulate disease-causing immune cells in order to treat MS. In this context, dendritic cells (DC) are set forth as interesting cellular targets. Post-mortem studies of MS brains as well as studies in animal models suggest that migration of DC from the bloodstream through the blood-brain barrier (BBB) and subsequent accumulation of these cells in the brain parenchyma represent crucial events in MS pathogenesis. Hence, DC and the process of DC migration are interesting targets for the development of new therapeutic strategies. Here, we will study the transmigratory capacity of circulating DC from MS patients using an in vitro BBB model. By studying differences in phenotype and function between migrating and non-migrating DC from MS patients and healthy controls, we aim to identify new therapeutic targets in order to interfere with DC recruitment to the brain. Ultimately, this will allow us to generate tolerogenic DC exhibiting enhanced migratory capacity, with the potential to suppress ongoing myelin-specific responses in the central nervous system.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Multiple sclerose (MS) is een chronische inflammatoire auto-immuunaandoening van het centrale zenuwstelsel (CZS). Deze neurodegeneratieve ziekte wordt gekenmerkt door multifocale inflammatie, demyelinatie, axonale degeneratie en astrogliosis.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Multiple sclerosis (MS) is the leading cause of non-traumatic disability in young adults. Although growing insights into disease mechanisms underlying MS have resulted in the development of new therapeutic strategies, none of the currently available treatments results in permanent stabilization or cure of MS. Current research efforts are focused on further unraveling MS immunopathogenesis as well as on finding ways to specifically manipulate disease-causing immune cells in order to treat MS. In this context, dendritic cells (DC) are set forth as interesting cellular targets. Post-mortem studies of MS brains as well as studies in animal models suggest that migration of DC from the bloodstream through the blood-brain barrier (BBB) and subsequent accumulation of these cells in the brain parenchyma represent crucial events in MS pathogenesis. Hence, DC and the process of DC migration are interesting targets for the development of new therapeutic strategies. Here, we will study the transmigratory capacity of circulating DC from MS patients using an in vitro BBB model. By studying differences in phenotype and function between migrating and non-migrating DC from MS patients and healthy controls, we aim to identify new therapeutic targets in order to interfere with DC recruitment to the brain. Ultimately, this will allow us to generate tolerogenic DC exhibiting enhanced migratory capacity, with the potential to suppress ongoing myelin-specific responses in the central nervous system.
  Onderzoek - Universitei...  
Show textShow cached sourceOpen source URL
Vernietigende inflammatoire responsen in het centrale zenuwstelsel (CZS) zijn een kenmerk van neurodegeneratieve pathologieën, met multiple sclerosis (MS) en hersentrauma als uitstekende voorbeelden die de complexe interactie aantonen tussen CZS microglia en letsel-infiltrerende leukocyten.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine uantwerpen.be as primary domain
Detrimental inflammatory responses in the central nervous system (CNS) are a hallmark of various neurodegenerative pathologies, with multiple sclerosis (MS) and stroke/trauma being excellent examples demonstrating the highly complex interplay between CNS resident microglia and lesion infiltrating leucocytes. Lesion-associated inflammatory responses, both in the acute as well as in the chronic phase, are classified as being highly pro-inflammatory. In this context, it is generally believed that a functional conversion of a pro-inflammatory type M1 microglia/macrophage phenotype, which can readily be detected in severe CNS inflammatory lesions, into a type M2a immune modulating microglia/macrophage phenotype can have a beneficial effect on disease outcome. Using our extensive experience with cell implantation into the CNS of mice, our current research aims at in vivo modulation of neuro-inflammatory responses by intracerebral implantation of mesenchymal stem cells (MSCs) genetically engineered to express interleukin (IL)13, a potent inducer of the M2a phenotype in macrophages. Thus far, we have demonstrated in the cuprizone (CPZ) mouse model of CNS inflammation and demyelination that microglial quiescence and subsequent protection against demyelination coincides with the appearance of M2a-polarised macrophages in the CNS following grafting of IL13-expressing MSCs. Continuing our research, this PhD project will focus on unravelling the in vivo signalling events that lead to IL13-mediated induction of the M2a macrophage phenotype within MSC graft-infiltrating macrophages in the CNS, as well as the cellular interactions by which these M2a macrophages can influence the development of microglia/macrophage-mediated neuro-inflammation in the CNS. Upon completion we hope to: (i) further elucidate the immunological consequences of MSC grafting in the CNS, and (ii) provide pre-clinical rationale for the use of IL13 as an immune modulating cytokine in the CNS.