Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0043167 (
pertussis
)
19,595
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The changed patterns of proteolytic activity in brain and spinal cord of Lewis rats were examined in 4 different morphological variants of EAE: ordinary induced by the standard emulsion, hyperacute induced by an emulsion plus
pertussis
vaccine, passive induced by donor EAE cells, and monocytic induced by treatment of passive EAE with the immunosupressive drug tilorone. The following enzymatic changes were found: firstly, in ordinary EAE there was a 2--3.5-fold increase in cathepsins A and C (E.C. 3.4.14.1) in spinal cord one day following the appearance of paralysis with a smaller change in hindbrain, and none in the forebrain regions. With recovery from paralysis, levels of cathepsin A remained high in upper cord, and
cathepsin C
levels fell to about half. In contrast, increase in cathepsin D(E.C. 3.4.23.5) was smaller and occurred only 4--5 days after paralysis with the largest change in spinal cord areas and with only a small decrease on recovery from paralysis. Secondly, in hyperacute EAE, the increase in all cases was smaller with the largest change in cathepsin A level in upper spinal cord. In passive EAE, the most significant increase occurred only in the lower spinal cord for cathepsins A and C, and fourthly, in monocytic EAE induced by tilorone, there was an exceptionally large, 3-fold increase in
cathepsin C
in lower cord as compared to a 1.5-2 fold increase for other cathepsins. No major differences were observed on comparison of antigens from different sources (guinea pig and bovin spinal cord myelin peptide). An attempt is made to relate enzymatic changes to the morphological features of each variant with special reference to the nature of the infiltrating cells.
...
PMID:Proteolytic enzymes in ordinary, hyperacute, monocytic and passive transfer forms of experimental allergic encephalomyelitis. 84 13