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  • Germany  (2)
  • Plasma renin activity  (2)
  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; SURVIVAL ; ENDOTHELIAL GROWTH-FACTOR ; Germany ; IN-VIVO ; MODEL ; MODELS ; PATHWAY ; PATHWAYS ; VITRO ; GENERATION ; VOLUME ; DEATH ; DISEASE ; DISEASES ; DRUG ; DIFFERENTIATION ; LIGAND ; MECHANISM ; RAT ; CELL-SURVIVAL ; CELL-DEATH ; LONG-TERM SURVIVAL ; TRANSIENT GLOBAL-ISCHEMIA ; STEM-CELLS ; CENTRAL-NERVOUS-SYSTEM ; COLONY-STIMULATING FACTOR ; STROKE ; signaling ; ADULT ; FOCAL CEREBRAL-ISCHEMIA ; NEURONS ; cell survival ; CEREBRAL-ISCHEMIA ; NEURAL STEM-CELLS ; cell death ; progenitor ; FUNCTIONAL RECOVERY ; MATURE ; RECOVERY ; NEURONAL DIFFERENTIATION ; HIPPOCAMPAL-NEURONS ; FACTOR G-CSF ; INFARCT ; NEWLY GENERATED NEURONS ; RAT DENTATE GYRUS
    Abstract: G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong antiapoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neuronal differentiation in vitro. G-CSF markedly improved long-term behavioral outcome after cortical ischemia, while stimulating neural progenitor response in vivo, providing a link to functional recovery. Thus, G-CSF is an endogenous ligand in the CNS that has a dual activity beneficial both in counteracting acute neuronal degeneration and contributing to long-term plasticity after cerebral ischemia. We therefore propose G-CSF as a potential new drug for stroke and neurodegenerative diseases
    Type of Publication: Journal article published
    PubMed ID: 16007267
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  • 2
    Keywords: RECEPTOR ; APOPTOSIS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; IN-VITRO ; Germany ; IN-VIVO ; MODEL ; MODELS ; THERAPY ; VITRO ; VIVO ; DISEASE ; GENE ; DRUG ; DIFFERENTIATION ; MICE ; MRI ; BIOLOGY ; TARGET ; MOUSE ; TRANSGENIC MICE ; FIBER ; INSTABILITY ; LENGTH ; NEURITE OUTGROWTH ; INJURY ; G-CSF ; DEFICIENT MICE ; FOCAL CEREBRAL-ISCHEMIA ; HIPPOCAMPAL ; FUNCTIONAL RECOVERY ; spinal cord injury ; HIPPOCAMPAL-NEURONS ; FACTOR G-CSF ; regeneration ; outcome ; SPINAL-CORD-INJURY ; CORTICOSPINAL TRACT ; hematopoietic growth factor ; MANGANESE-ENHANCED MRI ; MOTOR FUNCTION ; PROMOTES RECOVERY ; RESONANCE-IMAGING MEMRI
    Abstract: P〉Granulocyte-colony stimulating factor (G-CSF) is a potent hematopoietic factor that drives differentiation of neutrophilic granulocytes. We have recently shown that G-CSF also acts as a neuronal growth factor, protects neurons in vitro and in vivo, and has regenerative potential in various neurological disease models. Spinal cord injury (SCI) following trauma or secondary to skeletal instability is a terrible condition with no effective therapies available at present. In this study, we show that the G-CSF receptor is up-regulated upon experimental SCI and that G-CSF improves functional outcome in a partial dissection model of SCI. G-CSF significantly decreases apoptosis in an experimental partial spinal transsection model in the mouse and increases expression of the anti-apoptotic G-CSF target gene Bcl-X-L. In vitro, G-CSF enhances neurite outgrowth and branching capacity of hippocampal neurons. In vivo, G-CSF treatment results in improved functional connectivity of the injured spinal cord as measured by Mn2+-enhanced MRI. G-CSF also increased length of the dorsal corticospinal tract and density of serotonergic fibers cranial to the lesion center. Mice treated systemically with G-CSF as well as transgenic mice over-expressing G-CSF in the CNS exhibit a strong improvement in functional outcome as measured by the BBB score and gridwalk analysis. We show that G-CSF improves outcome after experimental SCI by counteracting apoptosis, and enhancing connectivity in the injured spinal cord. We conclude that G-CSF constitutes a promising and feasible new therapy option for SCI
    Type of Publication: Journal article published
    PubMed ID: 20202082
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  • 3
    ISSN: 1432-1076
    Keywords: Congenital adrenal hyperplasia ; 21-Hydroxylase deficiency ; Active renin concentration ; Plasma renin activity ; Mineralocorticoid replacement therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In congenital adrenal hyperplasia (CAR) due to 21-hydroxylase deficiency, measurement of plasma renin activity (PRA) has been the method of choice in diagnosing salt loss and in monitoring adequacy of mineralocorticoid replacement therapy. Due to methodological problems in PRA determinations, direct immunoradiometric assays for the measurement of active renin concentration have been developed. We measured PRA and active renin concentrations simultaneously in 39 patients with CAH (30 salt-wasting, 9 simple virilizing) to evaluate the potential role of this new method in the management of this disease. PRA was determined with an enzymatic assay (sample volume: 2 × 1000 μl plasma), active renin concentration with a direct immunoradiometric assay (sample volume: 2 × 200 μl plasma or serum). We found a highly significant correlation between active renin and PRA in our patients (P 〈 0.001), as previously shown in healthy subjects. Active renin was as reliable as PRA to assess the quality of mineralocorticoid replacement.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1076
    Keywords: Key words Congenital adrenal ; hyperplasia ; 21-Hydroxylase ; deficiency ; Active renin concentration ; Plasma renin activity ; Mineralocorticoid replacement therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency, measurement of plasma renin activity (PRA) has been the method of choice in diagnosing salt loss and in monitoring adequacy of mineralocorticoid replacement therapy. Due to methodological problems in PRA determinations, direct immunoradiometric assays for the measurement of active renin concentration have been developed. We measured PRA and active renin concentrations simultaneously in 39 patients with CAH (30 salt-wasting, 9 simple virilizing) to evaluate the potential role of this new method in the management of this disease. PRA was determined with an enzymatic assay (sample volume: 2 × 1000 μl plasma), active renin concentration with a direct immunoradiometric assay (sample volume: 2 × 200 μl plasma or serum). We found a highly significant correlation between active renin and PRA in our patients (P 〈 0.001), as previously shown in healthy subjects. Active renin was as reliable as PRA to assess the quality of mineralocorticoid replacement. Conclusion In children, active renin determination is preferable to PRA determination because of methodological advantages and a smaller sample volume. It correlates well with PRA and determines the activation of the renin-angiotensin system as precisely as PRA. Active renin determination is useful in the surveillance of mineralocorticoid replacement therapy in CAH.
    Type of Medium: Electronic Resource
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