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  • 1
    Electronic Resource
    Electronic Resource
    Neurotrophic factors influence upregulation of constitutive isoform of heme oxygenase and cellular stress response in the spinal cord following trauma (2000)
    Springer
    Amino acids 19 (2000), S. 351-361 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Spinal cord injury ; Heme oxygenase ; Heat shock protein ; Carbon monoxide ; Growth factors ; BDNF ; IGF-1 ; Immunohistochemistry ; Cell injury ; Spinal cord edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of brain derived neurotrophic factor (BDNF) or insulin like growth factor-1 (IGF-1) on spinal cord trauma induced carbon monoxide (CO) production and cellular stress response was examined using immunostaining of the constitutive isoform of the hemeoxygenase (HO-2) enzyme and the heat shock protein (HSP 72 kD) expression in a rat model. Subjection of rats to a 5 h spinal trauma inflicted by an incision into the right dorsal horn at T10–11 segment markedly upregulated the HO-2 and HSP expression in the adjacent spinal cord segments (T9 and T12). Pretreatment with BDNF or IGF-1 significantly attenuated the trauma induced HSP expression. The upregulation of HO-2 was also considerably reduced. These results show that BDNF and IGF-1 attenuate cellular stress response and production of CO following spinal cord injury which seems to be the key factors in neurotrophins induced neuroprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070066
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A new antioxidant compound H-290/51 attenuates nitric oxide synthase and heme oxygenase expression following hyperthermic brain injury (2000)
    Springer
    Amino acids 19 (2000), S. 383-394 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Hyperthermia ; Heat stress ; Brain edema ; Nitric oxide synthase ; Heme oxygenase ; Oxidative stress ; H-290/51 ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Influence of a new anti-oxidant compound H-290/51 on expression of nitric oxide synthase (NOS) and heme oxygenase (HO) enzymes responsible for nitric oxide (NO) and carbon monoxide (CO) production, respectively was examined in the CNS following heat stress in relation to cell injury. Exposure of rats to 4 h heat stress at 38°C in a biological oxygen demand (BOD) incubator (relative humidity 50–55%, wind velocity 20–25 cm/sec) resulted in profound edema and cell injury in many parts of the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus and brain stem. Immunostaining of constitutive isoforms of neuronal NOS (nNOS) and HO-2 revealed marked upregulation in damaged and distorted neurons located within the edematous brain regions. Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before heat stress) significantly reduced the edematous swelling and cell injury and resulted in a marked attenuation of nNOS and HO-2 expression. These observations suggest that upregulation of NOS and HO is associated with cell injury, and the antioxidant compound H-290/51 is neuroprotective in heat stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070069
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Antioxidant compounds EGB-761 and BN-520 21 attenuate heat shock protein (HSP 72 kD) response, edema and cell changes following hyperthermic brain injury (2000)
    Springer
    Amino acids 19 (2000), S. 339-350 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Hyperthermia ; Heat stress ; Heat shock protein (HSP 72 kD) ; Edema ; Cell injury ; Antioxidants ; EGB-761-BN 52021
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Influence of the extract of Gingko biloba (EGB-761) and one of its constituent Gingkolide B (BN-52021) on hyperthermia induced cellular damage and heat shock protein (HSP 72 kD) response was examined in a rat model. Rats subjected to 4 h heat stress at 38°C in a biological oxygen demand (BOD) incubator (relative humidity 50–55%, wind velocity 20–25 cm/sec) resulted in profound edema and cell injury in many parts of the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus and brain stem. Immunostaining of HSP 72 kD showed marked upregulation in the damaged and distorted neurons located within the edematous area. Pretreatment with EGB-761 (50 mg/kg/day, p.o.) and BN-520 21 (2 mg/kg, p.o.) per day for 5 days significantly reduced HSP expression and attenuated cell damage. Our results show that EGB-761 and its component Gingkolide B (BN-52021) has the capacity to reduce edema and cell injury following hyperthermia and this effect of the compound is somehow associated with a reduction in cellular stress response as evidenced with a reduction in HSP expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070065
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Growth hormone attenuates alterations in spinal cord evoked potentials and cell injury following trauma to the rat spinal cord (2000)
    Springer
    Amino acids 19 (2000), S. 363-371 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Growth hormone ; Spinal cord injury ; Edema formation ; Spinal cord evoked potentials ; Spinal cord edema ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of exogenous rat growth hormone on spinal cord injury induced alterations in spinal cord evoked potentials (SCEP) and edema formation was examined in a rat model. Repeated topical application of rat growth hormone (20 μl of 1 μg/ml solution) applied 30 min before injuryand at 0 min (at the time of injury), 10 min, 30 min, 60 min, 120 min, 180 min, and 240 min, resulted in a marked preservation of SCEP amplitude after injury. In addition, the treated traumatised cord showed significantly less edema and cell changes. These observations suggest that growth hormone has the capacity to improve spinal cord conduction and attenuate edema formation and cell injury in the cord indicating a potential therapeutic implication of this peptide in spinal cord injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070067
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Spinal nerve lesion induces upregulation of constitutive isoform of heme oxygenase in the spinal cord (2000)
    Springer
    Amino acids 19 (2000), S. 373-381 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Nerve lesion ; Neuropathic pain ; Heme oxygenase ; Carbon monoxide ; Cell injury ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of carbon monoxide (CO) on chronic spinal nerve lesion induced spinal cord neurodegeneration was examined using immunohistochemical expression of the constitutive isoform of its synthesising enzyme, hemeoxygenase-2 (HO-2) in a rat model. Spinal nerve lesion at L-5 and L-6 level was produced according to the Chung model of neuropathic pain and rats were allowed to survive for 8 weeks. Sham operated rats, in which the spinal nerves were exposed but not ligated, served as controls. Ligation of spinal nerves in rats resulted in an upregulation of HO-2 expression which was most pronounced in the ipsilateral gray matter of the spinal cord compared to the contralateral side. In these rats, morphological investigations showed distorted neurons, membrane disruption, synaptic damage and myelin vesiculation. Sham operated rats did not show an upregulation of HO-2 expression and the structural changes in the spinal cord were absent. These observations strongly suggest that spinal nerve lesion is associated with an increased production of CO which is somehow contributing to the neurodegenerative changes in the spinal cord, not reported earlier.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070068
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    Paper (German National Licenses)
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