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  • 1
    ISSN: 0942-0940
    Keywords: Total body hyperthermia ; autoregulation ; blood-brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was designed to examine the influence of total body hyperthermia (TBHT) using an extracorporeal circuit with a heat exchanger on the cerebral blood flow (CBF), intracranial pressure (ICP), brain tissue pH, cerebral autoregulation and blood-brain barrier (BBB) permeability in dogs. The rectal temperature of the dow was raised to 41.5 °C, maintained at 41.5–42.0 °C for 2 hours (HT period) and then reduced to normothermia by cooling. Regional CBF was measured by the hydrogen clearance method before heating, during the HT period and after cooling. ICP and brain tissue pH were monitored during the TBHT treatment. Autoregulation of the CBF during the HT period was assessed by measuring the regional CBF and the ICP in a state of induced hypo- or hypertension. The influence of TBHT on BBB permeability was examined using an immunohistochemical technique. The regional CBF increased from 38.1±6.5 (mean±SD) to 49.1±9.8 ml/100 g/min and the ICP from 10.3±4.2 to 16.8±3.4 mmHg when TBHT was raised. These returned to normal values after cooling. The regional CBF and the ICP changed in parallel with drug-induced changes of mean arterial blood pressure during the HT period. These changes suggest that autoregulation of the CBF is paralysed during the HT period. Brain tissue pH decreased rapidly when the rectal temperature exceeded 41.0 °C. The pH was 7.18±0.05 during the HT period and was relatively stable. The pH returned to a normal value after cooling. Immunopositive stain for albumin was not observed in heated brain tissue except for the normally leaky pineal gland and the choroid plexus, indicating preservation of BBB during TBHT. These results suggest that brain oedema may occur easily due to paralysed cerebral autoregulation when the arterial blood pressure fluctuates excessively, so arterial blood presssure must be controlled strictly during TBHT.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 139 (1997), S. 678-683 
    ISSN: 0942-0940
    Keywords: Cerebral ischaemia ; hippocampus ; hypoxia ; delayed neuronal death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The objective of this study was to clarify whether pre-exposure to hypoxia influences neuronal death following transient cerebral ischaemia. Twenty gerbils were exposed to 10% oxygen in a chamber for 3 weeks. The other control gerbils (n = 20) were fed in normoxia for 3 weeks. Both carotid arteries in the neck were occluded with aneurysm clips for 5 minutes under halothane anaesthesia in 30 gerbils, recirculated and then fed in normoxia. Five animals in both groups were sacrificed before, and 2, 4, and 7 days after surgery. The animals were fixed with 4% paraformaldehyde and histological study was performed. Immunohistochemical study was also done with antibodies against basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF). The neuronal death in the hippocampus was more severe in the hypoxic group. Expression of both bFGF and VEGF was obvious in the cingulate cortex, corpus callosum and internal capsule before clipping in the hypoxic group, but not observed in the normoxic group before clipping. We observed the expression of both bFGF and VEGF widely in the brain at 2 and 4 days after recirculation in both groups. The expression in the hypoxic group was much more prominent than that in the normoxic group. These expressions were not observed at 7 days in both groups. Pre-exposure to hypoxia followed by transient cerebral ischaemia accelerated neuronal death in the hippocampus, and induced the more obvious expression of both VEGF and bFGF compared with those in the normoxic group.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Keywords: Transient forebrain ischaemia; delayed neuronal death; neuronal protection; calcium/calmodulin-dependent protein kinase II.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  To clarify the relation between neuronal protection against ischaemia and calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity, we investigated temporal alterations of the kinase activity in the hippocampus after transient forebrain ischaemia under neuroprotective conditions, employing the gerbil bilateral carotid artery occlusion model.  The hippocampal CA1 neuronal density at 2 hours after 5 minutes of forebrain ischaemia was 214.7±25.8 /mm (mean±S.D.), and did not differ from the control significantly; however, it decreased to 11.7±4.2 /mm at 7 days after the ischaemia. The neuronal density at 7 days after the ischaemia was 185.1±18.5 under the hypothermic conditions, 128.7±19.6 with the brief ischaemic pretreatment, 65.0±13.4 with administration of MK-801, and 20.5±4.2 with the repetitive hyperthermic pretreatment, respectively.  The Ca2+/calmodulin-dependent activity of CaM kinase II in the hippocampal cytosolic fraction was decreased to 47.5% of the control value at 2 hours after the ischaemia, when CA1 neuronal death was not observed. In contrast, the activity was 98.8% of the control under the hypothermic conditions, 91.4% with the brief ischaemic pretreatment, 71.2% with administration of MK-801, and 47.9% with the repetitive hyperthermic pretreatment, respectively.  These results indicated that the preservation of the Ca2+/calmodulin-dependent activity of cytosolic CaM kinase II after ischaemia parallelled the neuroprotective effect in the gerbil hippocampus. Thus, it is suggested that the preservation of the activity may be involved in the mechanism of neuronal protection against ischaemia.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 138 (1996), S. 84-89 
    ISSN: 0942-0940
    Keywords: Auditory brain stem response ; basilar artery ; ethanol ; endothelial cell damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study in mongrel dogs was designed to observe the effects of ethanol on both endothelial cells of the basilar artery and brain function. By use of sterile surgical technique, a super-selective catheter was placed in the proximal portion of the basilar artery in the dogs. Five dogs received 3 ml of 25% ethanol and 5 dogs received 3 ml of 50% of ethanol through the catheter over 2 minutes. The remaining 5 dogs received 3 ml of saline as a control. Auditory brain stem response (ABR) was monitored for 2 hours after ethanol infusion, and then perfusion-fixation was performed from the heart with 4% paraformaldehyde. The basilar artery was observed with scanning electron microscopy after routine procedures. The endothelial cells were intact in the control group. The 50% group showed a higher level of injury to the endothelium as well as a higher degree of platelet adhesion and fibrin clot formation compared with the 25% group. The extensive endothelial-cell damage subsequently caused thrombus formation. The ABR disappeared immediately after ethanol infusion in both ethanol groups, and recovered gradually in the 25% group, but did not re-appear during the time course of 2 hours in the 50% group. The ethanol less than 25% in concentration near the endothelium is considered to be safe as a transcatheter embolic agent with the attention to the central toxicity.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; ICAM-1 ; subarachnoid haemorrhage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to study how immune-inflammatory responses are involved in the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH), the kinetics of expression of the intercellular adhesion molecule 1 (ICAM-1), a ligand for the leucocyte adhesion receptor, were studied on the cerebral arteries following SAH in rats. The SAH was induced by intracisternal injection of arterial blood. The rats were sacrificed at specified times: immediately after induction of SAH to seven days after SAH. Cryostat sections of the basilar artery (BA) were prepared and incubated with anti-rat ICAM-1 antibody. Morphometric analysis of the BA revealed a significant narrowing of the luminal diameter on Day 2 following SAH. While in the non-treated normal animals, no nor only weak expression of ICAM-1 was observed on the endothelial layer of the BA, there was greater expression of ICAM-1 on the endothelial layer of the BA in SAH rats, and the expression was observed also in the medial layer of the artery from Day 2 to Day 5 following SAH. The present results indicate that SAH really causes responses in the cellular immunity not only in the endothelial layer, but also in the medial layer of the artery as a target of immune damage, which is presumed to be one of the important steps in the development of cerebral vasospasm.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 0942-0940
    Keywords: Keywords: Plasminogen activators; plasminogen activator inhibitor I; brain tumour invasion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the role of plasminogen activators (PAs) and their inhibitor (plasminogen activator inhibitor-1, PAI-1) in human brain tumours. The amounts of urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1), and the activity of u-PA and t-PA were determined by enzyme-linked immunosorbent assay (ELISA), and u-PA and PAI-1 were immunolocalized using monoclonal antibodies in human brain tumours and normal brain tissues. The tissues were surgically removed from 64 patients; normal brain tissue (5 cases), low-grade glioma (4 cases), high-grade glioma (17 cases), metastatic tumour (9 cases), meningioma (benign 12 cases, malignant 6 cases), acoustic schwannoma (11 cases). u-PA activity and u-PA and PAI-1 antigen levels were significantly elevated in malignant brain tumours (malignant meningiomas, high-grade gliomas, and metastatic tumours) and acoustic schwannomas but very low in benign meningiomas, low-grade gliomas and normal brain. There was no difference in t-PA antigen levels among normal and malignant tissues, however levels of t-PA activity were markedly decreased in metastastic tumours. All malignant brain tumour tissues showed positive immunostaining for u-PA and PAI-1, however, some tumour cells showed negative intensity while others showed strong intensity for these antibodies. This contrasts to the homogeneous staining pattern found in acoustic schwannoma. These findings indicate that malignancy in human brain tumours is associated with elevated levels of u-PA and PAI-1 and that an imbalance between these proteins in a micro-enviroment contributes (ascribes) to tumour cell invasion.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 204-206 (Mar. 1996), p. 539-544 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Asia Pty. Ltd.
    Nephrology 5 (1999), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Plant, cell & environment 20 (1997), S. 0 
    ISSN: 1365-3040
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Phytochrome apoproteins in angiosperms are encoded by a small gene family. Tomato (Solatium lycopersicum L.) serves well as a dicotyledonous model system for elucidating the extent of this gene family, its expression patterns, and the roles of individual members of the family. Five phytochrome genes (PHYA, PHYB1, PHYB2, PHYE and PHYF have been characterized in tomato. Quantitative measurements of transcript abundances from each tomato PHY throughout the life cycle indicate that transcript levels generally range from 10 to 100 μmol mol−1 total mRNA, in the following order of decreasing abundance: PHYA, PHYB1, PHYE, PHYB2 and PHYF. PHYA transcripts were found to be most abundant in seedling roots, while PHYB2 and PHYF transcripts were expressed preferentially in fruit. PHYA mutants (fri) have been found to be the consequence of a single nucleotide substitution adjacent to the 3′ terminus of an intron. What are almost certainly PHYB1 mutants have also been described, although the molecular nature of these mutants remains to be revealed. Efforts to obtain PHYB2, PHYE and PHYF mutants are currently underway.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Chester : International Union of Crystallography (IUCr)
    Journal of synchrotron radiation 6 (1999), S. 439-441 
    ISSN: 1600-5775
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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