To identify the cellular targets of TNF alpha in human gliomas, a total of 30 surgical specimens (12 glioblastomas, 4 anaplastic astrocytomas, 3 astrocytomas, 7 brains adjacent to tumour (BAT), 4 histologically normal-appearing brains) were examined by in vitro binding technique using biotinylated TNF alpha. The TNF-binding sites (TNF-BS) were recognized in the tumour cells in 8 of the 12 glioblastomas, 3 of the 4 anaplastic astrocytomas and in all the 3 astrocytomas. The TNF-BS were also recognized in the vascular endothelial cells in all these cases. The presence of TNF-BS in blood vessels ranged from 7.7 to 74.4% of the background vessels. This wide range of variation in the presence of TNF-BS within the tumour cells and tumour blood vessels may be relevant to the variable response of individual tumours to TNF alpha therapy. Since the tissue of normal brain, which lacks TNF-BS, might hardly be affected by this cytokine, administration of TNF alpha may be considered as an adjuvant therapy in selected groups of patients.
Cyclocopolymerizations of maleic anhydride (1) with 1,Shexadiene ( 2 4 and 2,Sdimethyl-1,Shexadiene (2 b) were compared with those of 1 with 1,edienes which have been reported to yield highly cyclized polymers following a bimolecular alternating inter-intramolecular mechanism. The mole ratio of monomeric units of 1 to those of the dienes in the copolymers was almost 2 : 1, though it changed slightly with the monomer composition in the feeds. Although the fundamental aspect of the copolymerization of 1 with 1,5-dienes was found to be similar to that with 1,4dienes, the structures of the copolymers are different from those obtained with 1 ,Cdienes in that not only pendant double bonds, but also other unsaturations were detected. The unsaturations were formed by combination of propagating radicals with the ally1 radical, which is considered to be formed by hydrogen abstraction from the penultimate hexenyl group. A mechanism is proposed to explain the degree of cyclization and the copolymer composition.
A conditioned medium from cultured human epidermal cells was observed to inhibit the activity of exogenous urokinase. By reverse fibrin autography after SDS polyacrylamide gel electrophoresis, a plasminogen activator inhibitor was detected with a molecular weight of 46,000. Using Mr 33,000 [125I]-labelled urokinase we observed the formation of an enzyme-ligand complex. The molecular weight of this complex was 79, 000. These results indicate that cultured human epidermal cells secrete a plasminogen activator inhibitor (urokinase inhibitor) with a molecular weight of 46,000.
Reactivity of scleroderma fibroblasts to lymphoid cell-derived fibroblast growth factor (FGF) was assessed in this study. The fibroblasts from the sclerotic lesion failed to respond to FGF, whereas those from scleroedematous lesions responded equally to normal fibroblast. Response of the fibroblast from sclerotic lesion was also lower than that of the fibroblast from mature scar. Fibroblasts obtained from three different layers of healthy skin, papillary dermis, reticular dermis, and reticular-subcutaneous layer, responded equally to FGF, whereas the fibroblast of reticular dermis from sclerotic lesion failed to respond to FGF. It is suggested that the fibroblast of reticular dermis in scleroderma is variously activated by some unknown factors, so that they do not have enough reserve to respond to further stimuli.
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