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1.
Eur J Vasc Endovasc Surg ; 50(1): 94-100, 2015 Jul.
Article in English | MEDLINE | ID: mdl-25985890

ABSTRACT

OBJECTIVES: The COhorte de Patients ARTériopathes (COPART) Risk Score is a risk score assessing the 1 year outcome of patients who received inpatient treatment because of their peripheral arterial occlusive disease (PAOD). The COPART Risk Score consists of six variables each of which is allocated a different number of points (age, history of myocardial infarction, C-reactive protein, ankle-brachial index, estimated glomerular filtration rate, medication with antiplatelet agents, statins and renin-angiotensin system inhibitors). METHODS: 129 consecutive claudicants were included in a prospective trial with an average follow up of 8.8 (± 0.7) years. All patients were hospitalized for their first endovascular procedure to the pelvic and/or femoropopliteal arteries. The endpoints were all cause mortality and cardiovascular (CV) death. The COPART Risk Score was calculated for the three patient cohorts (low risk: 52 patients [40.3%]; medium risk: 41 patients [31.8%]; high risk: 36 patients [27.9%]). RESULTS: During the follow up period 23.1% (n = 12) of patients in the low risk group, 34.1% (n = 14) of patients in the medium risk group, and 63.9% (n = 23) of patients in the high risk group died. CV death occurred in 11.5% in the low, 22.0% in the medium, and 41.7% in the high risk groups. The three groups differed significantly with regard to all cause and CV mortality (p < .0001 and p = .001). CONCLUSIONS: The COPART Risk Score is a suitable instrument to predict long-term all cause and CV mortality in claudicants preceding their first peripheral intervention.


Subject(s)
Arterial Occlusive Diseases/mortality , Leg/blood supply , Peripheral Arterial Disease/mortality , Aged , Aged, 80 and over , Cohort Studies , Female , Humans , Male , Middle Aged , Prospective Studies , Risk Assessment , Time Factors
3.
Praxis (Bern 1994) ; 90(8): 293-6, 2001 Feb 22.
Article in German | MEDLINE | ID: mdl-11256330

ABSTRACT

Malignant melanoma represents only 1.5-2.5% of malignant neoplasms in Europe. Since 1990 the clinical data of melanoma patients are registered at the clinic for dermatology university Düsseldorf. 925 patients were treated between 1990-1996 (not including in situ melanomas, extracutaneous melanomas and multiple melanomas). In 1996 the incidence was 15 cases/100,000 habitants. A worldwide doubling of the morbidity is expected every ten years especially in the caucasian population.


Subject(s)
Melanoma/epidemiology , Skin Neoplasms/epidemiology , Urban Population/statistics & numerical data , Adolescent , Adult , Aged , Aged, 80 and over , Child , Cross-Sectional Studies , Female , Germany/epidemiology , Humans , Incidence , Male , Middle Aged
4.
Biochem Pharmacol ; 50(3): 381-90, 1995 Jul 31.
Article in English | MEDLINE | ID: mdl-7646539

ABSTRACT

Previous results demonstrated that incubation of the Friend murine erythroleukemic cell with 5 microM AZT for several days leads to a decrease in the rate of cell growth, inhibition of mtDNA replication, reduction of mtDNA per cell and per mitochondrion, and an increase in mitochondria per cell. As shown here, such treatment also leads to changes in lactate and ATP synthesis and in O2 uptake, suggesting impairment of oxidative phosphorylation. Direct measurement of ATP synthesis in mitochondria isolated from AZT-treated cells confirmed this view. The most significant new finding in this paper, however, is that in addition to these delayed effects of AZT, similar but very rapidly appearing effects on oxidative phosphorylation were noted, with changes observed in the above parameters including mitochondrial proliferation. Some of these occurred as early as 3 hr, only 7% of the doubling time, after exposure of the cells to 5 microM AZT, a period too short for initiation of appreciable mtDNA-mediated effects. Studies on isolated mitochondria provided no evidence of the identity of the immediate target of AZT: AZT does not act as an uncoupler or inhibitor of respiratory control, and previous results failed to implicate adenylate kinase. We have also begun to address the question of the mechanism of AZT-induced mitochondrial proliferation. Initial experiments showed that AZT inhibited synthesis of total cytosolic protein but stimulated synthesis of those proteins imported into mitochondria from the cytoplasm. We also report that aminothymidine, a catabolite of AZT in liver capable of inhibiting cell growth, was not generated by Friend cells.


Subject(s)
Mitochondria/drug effects , Oxidative Phosphorylation/drug effects , Zidovudine/pharmacology , Adenosine Triphosphate/metabolism , Animals , Cell Division/drug effects , Cell Line , Cytosol/drug effects , DNA Replication/drug effects , DNA, Mitochondrial/drug effects , Dideoxynucleosides/metabolism , Lactates/metabolism , Lactic Acid , Mice , Mitochondria/metabolism , Oxygen/metabolism , Protein Biosynthesis , Time Factors
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