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  • 1
    ISSN: 0942-0940
    Keywords: Chronic subdural haematoma ; histochemistry ; PAF-acetylhydrolase ; platelet-activating factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Platelet activating factor (PAF) content and PAF-acetylhydrolase (PAFAH) activity were measured in the plasma and haematoma of 34 chronic subdural haematoma (CSH) patients. The plasma PAF level in patients with CSH was higher than that in healthy controls. Although there was no correlation between the plasma PAF levels and the interval between the onset of symptoms and the day of sampling, namely, the interval after bleeding, the haematoma PAF level gradually decreased according to the interval after the onset of symptoms. There was no difference between plasma PAFAH activity in patients with CSH and that in healthy controls, and haematoma enzyme activity gradually increased correlated with the interval between the onset of symptoms and surgery. In addition, the localization of PAF in haematoma capsules was histochemically determined. PAF was solely localized to the peri-sinusoidal vessels in the outer membrane of haematoma capsules. Based on these biochemical and histochemical studies, we speculated that PAF may play a role in the development of chronic subdural haematomas.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Brain tumour ; PDGF-B ; platelet factor 4 ; tumour marker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The plasma concentration of the platelet-derived growth factor (PDGF)-B chain and the plasma platelet factor 4 (PF4) levels were measured in 17 healthy controls and 55 brain tumour patients. In the 17 normal controls, the plasma PDGF-B and PF4 levels were 523 ± 157 pg/ml (mean ± SD) and 84 ± 37 ng/ml, respectively. In the brain tumour patients, these values were 881 ± 854 pg/ml and 93 ± 64 ng/ml, respectively. The plasma PDGF-B concentration was elevated above the upper limit of normal individuals in 12 (22%) of the 55 patients. However, since the corresponding PF4 levels suggested the platelet activation, the increased plasma PDGF-B may have originated from platelets. To address this, platelet releasing experiments were performed on citrated blood samples from 5 normal individuals. The plasma PDGF-B and PF4 levels from the 17 normal controls and those observed in the platelet releasing experiments correlated with a regression line of Y = 240 + 4.86X (Y: PDGF, X: PF4). There were only 6 (11%) patients whose plasma PDGF-B level was elevated above the 95% confidence limit estimated from the corresponding PF4 value. In these patients, the tumour volumes were extensively large, and those elevated PDGF-B values decreased after treatment and became elevated again in three patients with recurrent glioblastoma. Although the plasma tumour-derived PDGF-B was detected only in an extensively large brain tumour, it might be a useful plasma marker evaluating the effects of therapy and prognosis in such patients.
    Type of Medium: Electronic Resource
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