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  • 1
    Electronic Resource
    Electronic Resource
    Identification of p-57, a serine proteinase, from human erythrocyte membranes, which cleaves both chains of human third component (C3) of complement
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 140 (1986), S. 1113-1120 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0006-291X(86)90750-3
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  • 2
    Electronic Resource
    Electronic Resource
    Rapid Communication: Regional Variability in DNA Fragmentation After Global Ischemia Evidenced by Combined Histological and Gel Electrophoresis Observations in the Rat Brain (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have studied whether the delayed cell death induced by transient forebrain ischemia is associated with an inter-nucleosomal cleavage of DNA into oligonucleosome-sized fragments. The integrity of genomic DNA in various brain regions after a 20-min four-vessel ischemia was examined using gel elec-trophoresis. We found typical ladders of oligonucleosomal DNA fragments in the striatum and in the Ammon's horn. In the latter we also often found a random DNA degradation as a smear pattern. These findings were reinforced by a specific in situ labeling of DNA breaks in tissue sections. A dark staining of nuclei was observed in the cell bodies of neurons—in particular in the head of the caudate and in the vulnerable CAl hippocampal area. With biochemical and histological approaches, there was no evidence of DNA degradation in regions that are resistant to the injury. We conclude that the association of multiple mechanisms of cell damage may occur after a global ischemia. The regional variability in DNA fragmentation stresses the importance of using histological approaches in parallel with gel electrophoresis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb09843.x
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  • 3
    Electronic Resource
    Electronic Resource
    Poly(ADP-Ribose) Synthase Inhibition Reduces Ischemic Injury and Inflammation in Neonatal Rat Brain (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Poly(ADP-ribose) synthase (PARS), an abundant nuclear protein, has been described as an important candidate for mediation of neurotoxicity by nitric oxide. However, in cerebral ischemia, excessive PARS activation may lead to energy depletion and exacerbation of neuronal damage. We examined the effect of inhibiting PARS on the (a) degree of cerebral injury, (b) process of inflammatory responses, and (c) functional outcomes in a neonatal rat model of focal ischemia. We demonstrate that administration of 3-aminobenzamide, a PARS inhibitor, leads to a significant reduction of infarct volume: 63 ± 2 (untreated) versus 28 ± 4 mm3 (treated). The neuroprotective effects currently observed 48 h postischemia hold up at 7 and 17 days of survival time and attenuate neurological dysfunction. Inhibition of PARS activity, demonstrated by a reduction in poly(ADP-ribose) polymer formation, also reduces neutrophil recruitment and levels of nitrotyrosine, an indicator of peroxynitrite generation. Taken together, our results demonstrate that PARS inhibition reduces ischemic damage and local inflammation associated with reperfusion and may be of interest for the treatment of neonatal stroke.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0742504.x
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  • 4
    Electronic Resource
    Electronic Resource
    Increase in Specific Proteins and mRNAs Following Transient Anoxia-Aglycaemia in Rat CA1 Hippocampal Slices (1992)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 4 (1992), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Incorporation of [35S]methionine into proteins and two-dimensional gel autoradiograms was used to characterize early post-anoxia–aglycaemia protein synthesis in the CA1 area of rat hippocampal slices maintained in vitro. We have compared the effects of 3–4 min and 5–10 min insults, since the former but not the latter produces a reversible block of synaptic transmission (see companion paper). An insult of between 3 min 30 s and 4 min induces a transient increase in the labelled proteins during the first hour of reoxygenation, as compared to control. The increase in protein synthesis is conspicuous for several proteins, including actin, α-tubulin and heat-shock proteins (hsp70c and hsp90), as determined by immunoblotting. In the case of α-tubulin, we show with in situ hybridization and polymerase chain reaction procedures that the increase in protein synthesis is associated with a marked increase in the expression of the corresponding messenger RNAs. The results demonstrate that, in addition to regulatory proteins such as hsps, the synthesis of several polypeptides, including those associated with the cytoskeleton, is altered in anoxic damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1992.tb00186.x
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  • 5
    Electronic Resource
    Electronic Resource
    Nitric Oxide Production and Perivascular Tyrosine Nitration Following Focal Ischemia in Neonatal Rat (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Oxygen free radicals and nitric oxide (NO•) have been proposed to be involved in acute CNS injury produced by cerebral ischemia; however, controversy remains regarding how they cause injury. Because superoxide generation is triggered during reperfusion, the cytotoxic oxidant peroxynitrite could be formed, but it is not known if this occurs. Dot blot and immunohistochemistry studies were performed on the magnitude and time course of tyrosine nitration and inducible NO synthase (NOS2) in the postischemic rat pup brain. Neonatal ischemia was induced by permanent left middle cerebral artery occlusion in association with 1-h occlusion of the left common carotid artery in 7-day-old Wistar pups. Nitrotyrosine (NT) immunoreactivity was evident in the blood vessels close to the cortical infarct at 48–72 h of recovery, and T lymphocytes were involved with this production. NOS2 immunoreactivity was seen in neutrophils in the same vessels and in the parenchyma at 72 h of recirculation. Whereas NT staining decreased with time, NOS2-positive neutrophils could be still detected in arachnoid vessels at 14 days of recirculation. We conclude that perivascular reactions mediated by peroxynitrite are important in the cascade of events that lead to brain oxidative stress in neonatal ischemia. Moreover, NO-related species may serve as a signaling function instead of directly mediating toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70062516.x
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  • 6
    Electronic Resource
    Electronic Resource
    Regulation of apoptosis-associated proteins in cell death following transient focal ischemia in rat pups (1997)
    Springer
    Apoptosis 2 (1997), S. 368-376 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; Bax ; Bcl2 ; cerebral neonatal ischemia ; hsp72 ; immunohistochemistry ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis is a process whereby developmental or environmental stimuli activate a genetic programme to execute a specific series of events that culminate in the death and efficient disposal of a cell. Although a series of recent data suggested that neuronal death following cerebral ischemia occurs through an apoptotic pathway, additional work is needed to establish the existence of a causal relationship between gene expression and DNA breaks in neuronal death. We investigate the role of p53 and Bax proteins in the induction of apoptosis induced by a new transient focal ischemia model in the rat pup. Our results show that wild-type p53 exerts a significant and time-dependent effect in the initiation of apoptosis, and that apoptosis is induced via DNA-strand breakage. Subsequently, increased Bax expression was observed in the cytoplasm of dying cells located in the infarct, whereas an increased Bcl-2 and hsp72 staining was detectable in survival cells and reactive glia present at the periphery of the lesion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026453623753
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  • 7
    Electronic Resource
    Electronic Resource
    Ultrastructural Morphology of Neuronal Death Following Reversible Focal Ischemia in the Rat (1998)
    Springer
    Apoptosis 3 (1998), S. 133-141 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cerebral ischemia ; electron microscopy ; necrosis ; TUNEL staining
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Electron microscopy and terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labelling (TUNEL) were used to illustrate the different stages and subcellular alterations of cell degeneration that occur in the striatum of the rat after transient focal ischemia. Degenerating neurons exhibited different morphological types: apoptosis Type 1 (aggregation of dense masses of chromatin beneath the 'intact' nuclear membrane) and Type 2 (high cytoplasmic vacuolization), and necrosis. These profiles were localized in different part of the striatum. Type 1 was found in the head of the caudate putamen, Type 2 in the middle part of the striatum and necrosis in the striatal core. These ultrastructural results demonstrated that apoptosis occurs in neurons following focal ischemia in the striatal penumbra. In contrast, necrosis can be observed in the ischemic core, the region maximally affected by the ischemia. Finally, the presence of astrocytes throughout both the penumbra and ischemic core displaying numerous cytoplasmic vacuoles suggested an activation of glial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009653126347
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  • 8
    Electronic Resource
    Electronic Resource
    Release of endogenous excitatory amino acids and proteins by the mast cell degranulating peptide in the hippocampus (1989)
    Springer
    Pflügers Archiv 414 (1989), S. S123 
    Details
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582261
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  • 9
    Electronic Resource
    Electronic Resource
    Reactive astrocytes in the kainic acid-damaged hippocampus have the phenotypic features of type-2 astrocytes (1993)
    Springer
    Journal of neurocytology 22 (1993), S. 299-310 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Kainic acid treatment, a model of temporal lobe epilepsy, induces Ammon's horn sclerosis characterized by degeneration of CA3 pyramidal neurons and reactive gliosis. We now report that in kainic acid treated rats, reactive astrocytes in the hippocampus are A2B5 immunopositive and express GAP-43 immunoreactivity. A2B5 is a cell surface ganglioside selectively expressed in the glial O-2A lineage (oligodendrocytes and type-2 astrocytesin vitro). Since A2B5-positive cells were also GFAP immunoreactive, our observations suggest that hippocampal-reactive astrocytes in the epileptic process are type-2 astrocytes. GAP-43 is a membrane-associated phosphoprotein involved in neurite outgrowth.In vitro analysis showed that the glial O-2A lineage may express this phosphoprotein. In this study, we found that GAP-43 was coexpressed in astrocytes with A2B5 suggesting thatin vivo asin vitro type-2 astrocytes express GAP-43.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01187128
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