Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Central neurocytoma: immunohistochemical and ultrastructural study (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 418-427 
    Details
    ISSN: 1432-0533
    Keywords: Neurocytoma ; Oligodendroglioma ; Synaptic vesicles ; Synaptophysin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eight cases of central neurocytomas were studied by immunohistochemistry and electron microscopy. Seven tumors were located in the lateral ventricles and one in the subependymal region. All but one patient had a favorable postoperative course. The tumors were composed of small uniform cells possessing amitotic round nuclei with frequent perinuclear halos, a few Homer Wright rosettes and no ganglion cells; an appearance resembling that of oligodendroglioma. Immunohistochemical studies disclosed neuron-specific enolase and Leu-7 positivity in all tumors, S-100 protein-positive cells were found in six, while glial fibrillary acidic protein —and vimentin-positive cells were confined to the blood vessels. Myelin basic protein as well as neurofilament were not detected in the tumors. Synaptophysin-positive areas were seen in one tumor. Ultrastructural examination showed distinctive neuronal tumor cells which had a cytoplasm with sparse dense-core vesicles and thin cell processes containing parallel microtubules. They were classified into three different types of tumor cells according to the extent of differentiation. The most consistent finding for histological diagnosis was the presence of typical or abortive synapses with clear and dense-core vesicles. Additionally, synaptophysin may be a specific marker for some central neurocytomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293463
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The influence of total body hyperthermia on brain haemodynamics and blood-brain barrier in dogs (1995)
    Springer
    Acta neurochirurgica 135 (1995), S. 62-69 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF02307416
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Transient cerebral ischaemia in mongolian gerbils pre-exposed to hypoxia (1997)
    Springer
    Acta neurochirurgica 139 (1997), S. 678-683 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01412004
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Alterations of Calcium/Calmodulin-Dependent Protein Kinase II Activity in Ischaemia-Induced Neuronal Death and Neuronal Protection Against Ischaemia in the Gerbil Hippocampus (1999)
    Springer
    Acta neurochirurgica 141 (1999), S. 287-294 
    Details
    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
    URL: http://dx.doi.org/10.1007/s007010050300
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Endothelial-cell injury of the basilar artery caused by ethanol infusion in dogs (1996)
    Springer
    Acta neurochirurgica 138 (1996), S. 84-89 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01411730
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Production of Urokinase-Type Plasminogen Activator (u-PA) and Plasminogen Activator Inhibitor-1 (PAI-1) in Human Brain Tumours (1998)
    Springer
    Acta neurochirurgica 140 (1998), S. 377-386 
    Details
    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
    URL: http://dx.doi.org/10.1007/s007010050112
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress (1991)
    Springer
    Archives of toxicology 65 (1991), S. 164-167 
    Details
    ISSN: 1432-0738
    Keywords: Methylmercury (MeHg) ; Catecholamines ; Hypoglycemic stress ; Sympathetic nervous system ; Nephrotoxicity ; Thyroidal functions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Five male Wistar rats were treated with methyl-mercury chloride (MMC) and compared with five agematched control rats. A dose of 10 mg/kg was given three times. The chronic effects of the MMC administration on the urinary output of catecholamines [norepinephrine (NE), epinephrine (E) and dopamine (DA)] were measured for 50 days. On the 69th day after MMC administration, the rats were examined for insulin-induced hypoglycemic stress. On the 90th day, the animals were decapitated and various organs were weighed and serum thyroid hormones [thyroid stimulating hormone (TSH) and total and free thyroxine (T4)] were measured. Decreases in DA excretion and DA response to stress were observed in the MMC-treated group. Inflammation of the kidney was also found, suggesting MMC-induced damage to the renal tubular region, the apparent site of renal DA synthesis. The MMC group and the control group showed differential NE and E response patterns. The lowered baseline excretion of NE appeared to continue even 70 days after MMC administration, while the difference in E excretion between the two groups disappeared 1 month after MMC administration. Both NE and E showed normal responsiveness to hypoglycemic stress induced by insulin. All serum TSH and total and free T4 baseline levels showed slight increases, and the thyroid gland weights in the MMC group were slightly heavier. These findings suggest a rather hyperthyroid state after the initial acute phase suppression, as suggested by the previous examinations. Thus, these findings suggest long-lasting effects of methylmercury administration, especially on renal DA synthesis. Baseline urinary excretion of NE and thyroid function could also be affected for a long time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02034946
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Abstracts (1995)
    Springer
    Journal of neuro-oncology 24 (1995), S. 125-139 
    Details
    ISSN: 1573-7373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01052669
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...