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Biomedical subjects

E Scheffler

Publications and source records attributed to E Scheffler.

10 recordsLinked to original sources
PubMed1995

[Successful use of a heparinoid (danaparoid sodium) for heparin-induced thrombocytopenia type II in aortic valve reoperation].

The 29-year-old, heroin-addicted patient received an aortic valve prosthesis (SJM) 10 years ago because of aortic valve stenosis III. One year after surgical treatment he refused to take Phenprocoumon and thus received no anticoagulation for 9 years. The patient was hospitalized due to cardial decompensation and thrombosis of the aortic valve prosthesis was diagnosed. Under heparinization, he developed heparin-induced thrombocytopenia type II, which disappeared after changing the medication to Danaparoid-Sodium. In order to avoid any further heparin exposure, we also carried out the surgical replacement of the aortic valve prosthesis under anticoagulation with Danaparoid-Sodium.

Adult↗
PubMed1994

Transgenic mice expressing human lipoprotein lipase driven by the mouse metallothionein promoter. A phenotype associated with increased perinatal mortality and reduced plasma very low density lipoprotein of normal size.

We have produced transgenic mice expressing human lipoprotein lipase (LPL) driven by the mouse metallothionein I promoter. We found that integration of the LPL gene construct was associated with a high perinatal mortality. Animals that survived the first 2 weeks of life grew normally afterwards. Compared with controls, transgenic animals had higher post-heparin plasma LPL and tissue LPL activities. Immunoreactive human LPL was detected in their post-heparin plasma but not in controls. Transgenic animals had significantly lower plasma very low density lipoprotein (VLDL) while on a regular laboratory chow. By electron microscopic analysis and nondenaturing polyacrylamide gradient gel electrophoresis, the size and morphology of the plasma VLDL were very similar in transgenic and control animals, which suggests that VLDL particles acted on by the increased tissue LPL in the transgenic animals were mostly taken up by the cell without being released back into circulation. The hypertriglyceridemia and elevated VLDL in response to sucrose feeding were completely abolished in transgenic animals. They also had lower VLDL lipids compared with control animals when they were fed a high-fat, high-cholesterol diet. Feeding the mother of transgenic mice a high-fat diet during pregnancy completely reversed the high perinatal mortality associated with the integrated transgene, which suggests that the deleterious effect of LPL overexpression may be related to the depletion of some essential lipid nutrient.

Animals↗
PubMed1994

Association between lipoprotein(a) and progression of coronary artery disease in middle-aged men.

The association between lipoprotein(a) (Lp[a]) and progression of coronary artery disease (CAD) compared with other serum lipids was evaluated in 104 patients with angiographically proven coronary atherosclerosis. Patients were randomized to either an intervention or a control group. The 12-month intervention program consisted of a low-fat diet and daily physical exercise. Patients in the control group received "usual care" by their private physician. Eighty-three patients (36 in the intervention and 47 in the control group) underwent repeat angiography after 1 year. Angiographically documented net regression was seen in 13 patients (8 in the intervention and 5 in the control group), no change was seen in 40 patients (21 in the intervention and 19 in the control group) and progression was noted in 30 patients (7 in the intervention and 23 in the control group). No correlation could be shown between Lp(a) and angiographically documented progression of the disease. In a multivariate analysis including metabolic variables, group assignment, age and smoking habits, only assignment to the intervention group (p = 0.0075) and a decrease in total cholesterol (p = 0.0167) were independently associated with the course of the disease. Patients with or without previous myocardial infarction (70 vs 34) did not differ in Lp(a) levels (median 9.15 vs 14.25 mg/dl). Patients with Lp(a) > 25 mg/dl were younger than patients with Lp(a) < or = 25 mg/dl (52 vs 55 years; p < 0.03), indicating a connection between Lp(a) and the development of premature CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1992

[Chronic coronary artery occlusion--age, morphology and chance of reopening. An attempt to define indications].

In chronic coronary occlusions the rate of successful reopening seems to be improved with the help of new techniques; the chance of success can be judged by the age of occlusion. Frequently this age cannot be fixed exactly. The purpose of the study was therefore to find out, whether the chance of reopening can be judged by morphology. 60 patients in whom the occlusions could not be passed with a conventional wire were treated with the ROTACS system. Cine angios were reviewed carefully, morphological details in at least two projections were evaluated in graphic representations and correlated with the acute success rate and the estimated age of occlusion. Morphological parameters associated with a higher rate of success (type A) were: 1) a clearcut proximal stump with 2) no sidebranches at the site of occlusion, 3) no bridging collaterals and 4) only a slight filling of the distal vessel. Parameters with a low success rate (type B) were: 1) no proximal stump, 2) sidebranches at the site of occlusion, 3) bridging collaterals and 4) a very good distal filling. 48/60 (80%) of occlusions could be classified in type A or type B. The success rate was 17/21 (81%) (type A) versus 5/27 (18.5%) (type B) (p < 0.0002). The estimated age of type B occlusions was significantly higher than in type A: median 8 versus median 4 months (p < 0.002). It is concluded that the rate of success in reopening chronic coronary occlusions can be judged in the majority of patients using morphological parameters.

Atherectomy, Coronary↗
PubMed1990

Alteration of plasma low density lipoprotein from smokers.

Thiobarbituric acid reactive substances (TBARS) in 38 low density lipoprotein (LDL) samples from 21 healthy male non-smokers and 17 smokers (greater than 20 cigarettes per day) were measured before and after oxidation. TBARS in the freshly isolated LDL from non-smokers and smokers were similar, however, oxidized LDL samples from smokers developed nearly twofold more TBARS than non-smoker LDL samples. 16 LDLs from 8 smokers and 8 non-smokers were conditioned in redox-metal containing F-10 medium and subsequently added to P 388 D.1 macrophage cultures. LDL dependent cholesteryl ester increase in the P 388 D.1 cells after an 18 h incubation with non-smoker LDL was significantly lower than in the cells incubated with smoker LDL (P less than 0.01). A higher reacylation rate of cholesterol in P 388 D.1 cells incubated with smoker LDL (P less than 0.05) suggests that LDL-cholesterol uptake is significantly higher in P 388 D.1 cells incubated with smoker-LDL than in P 388 D.1 cultures exposed to non-smoker LDL. This finding indicates that smoking might contribute to increased shunting of LDL into macrophages. The vitamin E content of 6 non-smoker LDL samples was significantly higher than that in 6 smoker-LDL samples (P less than 0.01). We conclude that the vitamin E/LDL ratio may differ significantly in heavy smokers and non-smokers.

Adult↗
PubMed1990

17 beta-estradiol inhibits LDL oxidation and cholesteryl ester formation in cultured macrophages.

The effects of 17 beta estradiol, testosterone, the estradiol benzoate, and probucol on the oxidation kinetics of low density lipoprotein (LDL) in vitro in absorption presence of 10 microM Cu (II) are examined. Changes in the absorption at 234 nm (A234) and fluorescence (Ex340/Em420) are monitored. The kinetics of the changes observed let us suggest a precursor-product relationship between dienes and fluorochromes in the oxidized LDL. The addition of 17 beta estradiol and probucol to LDL results in a prolongation of the lag phase characterized by only insignificant formation of dienes and fluorochromes. The addition of testosterone and estradiol benzoate used as control compounds has no effect on the lag phase and thus no LDL stabilizing effect. Conditioned LDL which was incubated in F-10 medium before exposure to cultured P388D.1 macrophages increases the formation of cytoplasmic lipid droplets and of cellular cholesteryl esters. The LDL stabilizing compounds beta estradiol and probucol (but not testosterone) causes a reduction of the cholesteryl ester content of the cultured macrophages. Protection of LDL particles against oxidative damage apparently results also in lowering of cytoplasmic cholesteryl ester in cultured P388D.1 cells. We conclude that the known antiatherosclerotic potency of 17 beta estradiol may in part result from its LDL stabilizing activity.

Animals↗
PubMed1989

Apolipoproteins in human amniotic fluid: concentrations, isoforms and polymorphism.

Apolipoproteins were determined in 50 human amniotic fluids obtained by amniocentesis during weeks 16 and 22 (n = 26) or 33 and 41 (n = 24) of gestation. Whereas apo A-I, A-II, A-IV, and E were identified at levels of 1, 0.7, 0.8 and 1% of normal human adult plasma, respectively, apo B levels were only 0.04% of plasma concentration and apo C-III levels were below the detection limits of the assay. Amniotic fluid levels of apo A-II, A-IV and E did not differ between early and late stages of pregnancy, but levels of apo B decreased and apo A-I increased significantly in late pregnancy. Isofocusing showed apo A-I, A-II and A-IV in identical positions as compared to human adult plasma. Furthermore the known genetic polymorphism of apo A-IV was detectable. Individuals heterozygous, for the variant form apo A-IV-2, showing the phenotype apo A-IV (2-1), had significantly higher levels of apo A-I and A-II as compared to the common phenotype apo A-IV (1-1). We conclude that human amniotic fluid contains the major plasma apolipoproteins at about 1% of plasma levels with the exception of apo B which shows a level at an order of magnitude less than high-density lipoprotein apoproteins in comparison to their plasma counterparts.

Amniotic Fluid↗
PubMedDate not supplied

Smoking influences the atherogenic potential of low-density lipoprotein.

The possible influence of smoking on the low-density lipoprotein (LDL) and its biological activity was investigated. Plasma LDL was prepared from healthy male smokers and nonsmokers, and oxidized with Cu (II) as prooxidant. Oxidized LDL from smokers generated significantly more lipid peroxidation products, so-called thiobarbituric acid reactive substances (TBARS), when compared to oxidized nonsmoker LDL. Analysis of vitamin E levels in LDL obtained from both smokers and nonsmokers revealed that the vitamin E content of smoker LDL was significantly less than that of nonsmoker LDL. The amounts of cholesteryl esters formed in cultured P388. D.1 macrophages were greater in the presence of smoker LDL than with nonsmoker LDL. The data suggest that some of the proatherogenic effects of smoking may be related to oxidative modification of LDL and alteration of its biological activity.

Adult↗