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:C0033377 (
prolapse
)
11,717
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The fibrinolytic activity in biopsy specimens of superficial veins obtained from postmenopausal women before and after treatment with a nonsteroidal estrogen (P 1496) was determined as well as the coagulation factors antithrombin 3 and components of the fibrinolytic system. Patients were given P 1496, 50 mg/day for 3 weeks before surgery for uterine
prolapse
. The prothrombin + factor 7 + factor 10 (P and P), factor 8, antithrombin 3, alpha-1-antitrypsin, anti(-2)-macroglobulin, and inhibitors of urokinase induced
plasminogen
activation were measured. Vein biopsy specimens were taken from the dorsal side of the hand. Fibrinolysis was measured after incubation. The fibrinolytic activity of the specimens was normal and unchanged with treatment.
...
PMID:Coagulative and fibrinolytic studies on postmenopausal women treated with a new non-steroidal oestrogen. 7 33
The family of matrix metalloproteinases (MMPs) is responsible for extracellular matrix degradation during physiological and pathophysiological tissue remodeling processes such as embryogenesis, tissue repair and cancer progression. Despite these important roles of MMPs, inhibition or ablation of individual members of the MMP family in animal models have been shown to have little effect. It has been speculated that this results from a functional overlap between individual MMPs and (as-yet-unclassified) functional overlaps between MMPs and other protease systems. We here present genetic data showing that concomitant ablation of MMP9 (gelatinase B) and the serine protease plasmin results in lethal inflammatory mass lesions in the colon. These lesions possessed several histological attributes that are characteristic of mucosal
prolapse
seen in humans, and they were found to be associated with splenomegaly, enlarged mesenteric lymph nodes, decreased thymus size and altered populations of circulating immune cells. A time-course study provided evidence that the massive lymphoid hyperplasia and reactive changes were secondary to discrete fibrinous lesions also observed in mice only deficient for
plasminogen
(Plg), the zymogen for plasmin. These data demonstrate a non-appreciated vital protective role for MMP9 in the absence of Plg.
...
PMID:MMP9 is protective against lethal inflammatory mass lesions in the mouse colon. 2112 24