CCL

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001-es BibID:BIBFORM041648
035-os BibID:PMID:2758320
Első szerző:Joó Ferenc (vegyész)
Cím:Inhibition by H-7 of the protein kinase C prevents formation of brain edema in Sprague-Dawley CFY rats / Ferenc Joó, Árpád Tósaki, Zoltán Oláh, Mátyás Koltai
Dátum:1989
Megjegyzések:The effect of the protein kinase C enzyme inhibitor H-7 was examined on the brain edema formation evoked by bilateral occlusion of the common carotid arteries in Sprague-Dawley rats of CFY strain. Brain edema was assessed by measurement of water and electrolyte contents of the brain. The results showed that pretreatment with H-7 reduced the extent of brain edema formation in a dose-dependent manner. The fact that H-7 treatment prevented the accumulation of water and certain electrolytes in the brain indicates that the protein kinase C may be activated not only in the neuronal structures but also in the microvessels during ischemia, which can lead directly or via certain calcium-mediated mechanisms to the opening of tight junctions resulting in the development of brain edema.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Brain Research 490 : 1 (1989), p. 141-143. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Oláh Zoltán Koltai Mátyás
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM048492
Első szerző:Szállási Árpád (pathológus)
Cím:Duration of desensitization and ultrastructural changes in dorsal root ganglia in rats treated with resiniferatoxin, an ultrapotent capsaicin analog / Arpad Szallasi, Ferenc Joo, Peter M. Blumberg
Dátum:1989
ISSN:0006-8993
Megjegyzések:We have previously demonstrated resiniferatoxin (RTX) to be an ultrapotent analog of capsaicin. Like capsaicin, RTX initially induces neurogenic inflammation, pain, and hypothermia and then causes desensitization of these responses. We examine here the duration of desensitization following acute treatment with the maximal tolerated dose of RTX. Desensitization to neurogenic inflammation began to diminish by 7 days, whereas desensitization to pain and to induction of hypothermia persisted for several weeks. Interestingly, a partial hypothermic response returned within 24 h if challenge was with RTX at 500-fold its ED50 for control animals; the animals, moreover, maintained their ability to thermoregulate in a hot environment. The time course of the morphological changes--ultrastructure and calcium staining--of dorsal root ganglion neurons was examined in parallel. The ultrastructural changes were evident by 4 h and persisted for the duration of the experiments. Limited calcium staining was visible at 12 and 24 h after treatment but then diminished. In comparison with capsaicin treatment, RTX caused more long-lasting desensitization as well as a distinct spectrum of response.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Dorsal root ganglion
Resiniferatoxin
Capsaicin analog
Desensitization
Megjelenés:Brain research. - 503 : 1 (1989), p. 68-72. -
További szerzők:Joó Ferenc (1949-) (vegyész) Blumberg, Peter M.
Internet cím:Szerző által megadott URL
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