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H Drexel

Publications and source records attributed to H Drexel.

At least 19 recordsLinked to original sources

Operating principle of an electron monochromator in an axial magnetic field.

Electron monochromators which are operated within an axial magnetic (guiding) field are especially suitable for the production of monochromatic electrons at low energies. Although in principle the technology of such devices has an appreciable historic background, we have discovered experimentally important new features, which cannot be understood using the previously published theories of operation. An in-depth study of the electron trajectories in a crossed electric and magnetic field using Simion1 showed a number of possible pitfalls, which have to be avoided in construction and operation. From our simulations we derived a novel design and operational method, which is currently under evaluation. We have already demonstrated that using this novel design an electron energy resolution of about 50 meV is realistic.

Electromagnetic Fields↗

R116C mutation of cationic trypsinogen in a Turkish family with recurrent pancreatitis illustrates genetic microheterogeneity of hereditary pancreatitis.

Hereditary pancreatitis is due to heterozygosity for gain-of-function mutations in the cationic trypsinogen gene which result in increased levels of active trypsin within pancreatic acinar cells and autodigestion of the pancreas. The number of disease-causing defects is generally considered to be low. To gain further insight into the molecular basis of this disorder, DNA sequence analysis of all five exons was performed in 109 unrelated patients with idiopathic chronic pancreatitis in order to determine the variability of the underlying mutations. Two German females and one German male were carriers of the most common N29I and R122H mutations (trypsinogen numbering system). In a Turkish proband, an arginine (CGT) to cysteine (TGT) substitution at amino acid position 116 was identified. Family screening demonstrated that the patient had inherited the mutation from his asymptomatic father and that he had transmitted it to both of his children, his daughter being symptomatic since the age of 3 years. In addition, a German male was found to be a heterozygote for a D100H (GAC-->CAC) amino acid replacement. Our data provide evidence for genetic heterogeneity of hereditary pancreatitis. The growing number of cationic trypsinogen mutations is expected to change current mutation screening practices for this disease.

Adult↗

Revascularization of residual viable myocardium improves left ventricular dysfunction in patients after myocardial infarction.

The symptoms and prognosis of patients after myocardial infarction are essentially influenced by left ventricular function. About 50% of infarct related segments contain partly viable myocardium. The aim of this study was to test the hypothesis that regional and global left ventricular function can be improved by revascularization of infarct related segments with residual myocardial viability. In 15 of 30 consecutive patients, residual viable myocardium was found in the affected segment within 2.2 +/- 1.6 months after AMI. Myocardial viability was estimated by exercise-redistribution-reinjection thallium scintigraphy (SPECT imaging). Rest and exercise radionuclide ventriculography was performed to measure regional and global left ventricular ejection fraction before and after revascularization of the infarct related artery. 10 +/- 3 months after revascularization we observed a significant increase in the regional left ventricular ejection fraction at rest (from 32 +/- 16% to 41 +/- 19%; p = 0.03), global left ventricular ejection fraction at rest (from 38 +/- 12% to 46 +/- 11%; p = 0.01), regional LV ejection fraction during exercise (from 34 +/- 16% to 46 +/- 20%; p = 0.01), and global left ventricular ejection fraction during exercise (from 38 +/- 14% to 49 +/- 14%; p = 0.02). The results show that after revascularization of infarct related segments with residual myocardial viability, the regional and global left ventricular ejection fraction may be significantly improved, both at rest and during exercise. Thus infarct related segments should be tested for residual viability. In its presence revascularization is recommended, as the left ventricular function may be markedly improved.

Aged↗

[Secondary prevention following coronary intervention. Survey of 13 intervention centers in Austria].

Risk factor control has been shown to reduce the incidence of coronary events in patients with or without preceding infarction. Secondary prevention should therefore be borne in mind by every cardiologist. In order to test this concept and/or to promote secondary prevention in our country, the following survey was conducted by our working group for epidemiology and prevention. All interventional centres of the country (7 million inhabitants) were asked to report relevant data of 50 consecutive patients with PTCA in a structured questionnaire. Thirteen centres responded and we report the data of 650 patients. The mean proportion of women was 28%, the mean age 61.1 years and the mean stent rate 49.8%. The indications for PTCA varied widely: stable angina 10-74%, unstable angina 10-86%, primary PTCA 0-22%. The risk factor history was distributed as follows: diabetes 12-46% (mean 22.3%), hypertension 32-68% (mean 54.2%), current smoking 6-56% (mean 21.9%), and total cholesterol (TChol) > 200 mg/dl: 30-78% (mean 60.3%). Current lipid values were available for T chol. in 44-100% (mean 84.5%) and for LDL in 4-100% (mean 67.1%). Dietary counselling by a dietician was done in 4-100% of patients (mean 35.6%) Information concerning the hazards of smoking was given to 25-100% (mean 83.6%) of current smokers. Drug treatment at hospital discharge was as follows: 84-100% (mean 93.1%) received ASA, 24-74% (mean 49.8%) ticlopidine, 6-84% (mean 53.3%) nitrates, 34-82% (mean 60.2%) beta blockers, 10-70% (mean 39.5%) ACE inhibitors, 4-74% (mean 4 7.2%) lipid lowering drugs, 7-48% (mean 17.8%) calcium antagonists, 0-12% (mean 6.1%) digitalis and 0-28% (mean 13.6%) diuretics. Follow-up data were collected in 4 centres at 6 months post discharge and were available for 174 patients. Here we found an increase in the prescription of calcium antagonists, digitalis and statins. The following conclusions were drawn at a conference in which all centres participated: lipid values should be available for each patient at PTCA, dietary counselling should be initiated for every patient during hospitalisation (and continued by the family physician) and the national cardiac society should promote guidelines for the use of drugs in which the variation in use is too wide at present. It should be ensured that these guidelines are implemented not only in patients after AMI but also in those after PTCA.

Adrenergic beta-Antagonists↗

[Leptospirosis (Weil's syndrome) with renal failure, severe jaundice, disseminated hemorrhages and xanthopsia].

We report a case of a 48-year-old man from western Austria with severe leptospirosis. This disease occurs worldwide but predominates in the tropics. The infectious urine of a wide variety of domestic and wild animals mediates transmission of the infection, which characteristically has a biphasic pattern. It begins with the "leptospiraemic phase" with high fever, conjunctival suffusion, muscle pain and headache. Hepatitis, nephritis and haemorrhages may follow. The second "immune phase" has a greater variety of clinical manifestations. Fever and the initial symptoms may recur and the central and peripheral nervous system may be involved. The patient reported showed all major characteristics except conjunctival suffusion. The outcome was favourable despite some conditions with a poor prognosis (jaundice, renal failure, haemorrhages). The extreme severity of jaundice and the xanthopsia (yellow vision) make the case unique.

Color Vision Defects↗

Deficiency of cholesteryl ester transfer protein. Description of the molecular defect and the dissociation of cholesteryl ester and triglyceride transport in plasma.

A patient is described who exhibited, despite excessively high postprandial triglyceride levels, high levels of HDL cholesterol. Measurement of CETP activity and mass in the patient's plasma showed values of less than 5% and 2%, respectively, of a normolipidemic plasma pool. The CETP cDNA of the patient exhibited a mutation (T-->G), turning codon 57 (TAT) of exon 2 into a stop codon (TAG) and abolishing a, XcmI restriction site. Digestion of directly amplified CETP cDNA from the patient with XcmI indicated the exclusive presence of CETP cDNA containing the mutation. Analysis of the corresponding region of the CETP gene indicated the patient to be heterozygous for the nonsense mutation at codon 57, a finding that can only be explained by the presence of a null allele in addition to the allele with the nonsense mutation. The combination of TG intolerance of uncertain cause, together with CETP deficiency due to a novel mutation, produced the paradoxical constellation--high levels of HDL cholesterol (172 mg/dL) associated with a high post-prandial lipemia of 1460 mg triglycerides/dL.8 hours--and provided further insight into the role of CETP as mediator between pools of triglycerides and cholesteryl esters in plasma.

Aged↗

Predictors of the presence and extent of peripheral arterial occlusive disease.

BACKGROUND: Data relating lipids to the angiographic presence and extent of atherosclerosis, as reported for the coronary circulation, are lacking for the peripheral site. METHODS AND RESULTS: This study comprised 102 patients with peripheral arterial occlusive disease (PAOD) referred for elective percutaneous transluminal angioplasty and 100 age-matched control subjects with normal coronary and peripheral angiograms. The presence of PAOD was defined as > or = 1 stenosis with > or = 50% narrowing, and the extent was defined as the total of > or = 50% lesions in the iliac, femoral, popliteal, and crural beds. The relation of lipids and nonlipid risk factors to the presence of PAOD was tested by stepwise logistic regression analysis; their relation to the extent of disease was analyzed by simple regression and stepwise discriminant analysis. The presence of PAOD was significantly and positively associated with LDL cholesterol (P = .0003), triglycerides (P = .0001), apolipoprotein B (P = .0073), and smoking (P = .005) and was significantly and negatively associated with HDL2 cholesterol (P = .0085) and apolipoprotein A-I (P = .021). In the logistic model, LDL cholesterol, triglycerides, smoking, and systolic blood pressure were selected as independent predictors of PAOD presence. The extent of PAOD was significantly and negatively correlated with HDL3 cholesterol (P = .005), HDL cholesterol (P = .013), and apolipoprotein A-I (P = .021) and was significantly and positively associated with smoking and fasting blood glucose. Age, smoking, and blood glucose were selected by the discriminant analysis as independent predictors of the extent of PAOD. CONCLUSIONS: From this large case-control study, it is concluded that the presence of PAOD is predicted by parameters of LDL, triglyceride, and HDL2 metabolism, whereas the extent of PAOD is related to HDL3 and nonlipid risk factors.

Adult↗

[Activity profile of beta blockers].

Beta-adrenergic blockers are heterogeneous with respect to their array of specific actions. Major characteristics of a compound's profile include beta-1 specificity, hydrophilicity, duration of action, antiarrhythmic potency, and intrinsic sympathomimetic activity (ISA). Hydrophilicity parallels duration of action, and beta-1 specificity is inversely related to the strength of metabolic effects. An ideal profile of a beta-adrenergic blocker encompasses high beta-1 specificity, long action, strong antiarrhythmic effects, and low ISA.

Adrenergic beta-Antagonists↗

Reversal of atherosclerotic obstructions by percutaneous transluminal angioplasty raises high-density lipoprotein cholesterol.

Variation of high-density lipoprotein cholesterol (HDL) levels in man show a strong inverse relationship to the incidence of atherosclerotic vascular disease. Conversely, effects of atherosclerosis and ischemia on lipoprotein metabolism are unclear. We investigated 41 patients, 10 women and 31 men, undergoing percutaneous transluminal angioplasty by measuring fasting lipoprotein cholesterol including high-density lipoprotein subfraction analysis before and one as well as 12 weeks after the procedure. Successful reopening of a haemodynamically significant iliac, femoral or popliteal obstruction was achieved in all patients. A highly significant (p < 0.001) increase of HDL cholesterol from 1.10 +/- 0.05 to 1.31 +/- 0.06 mmol/l was revealed 12 weeks later. This was due to a significant (p < 0.001) increase in HDL3 cholesterol by 26%, whereas HDL2 cholesterol did not change significantly. We conclude that HDL cholesterol levels increase after recanalization of a significant atherosclerotic obstruction which may be a direct effect of reperfusion or an indirect effect due to an increase in exercise tolerance.

Adult↗

[Lipid status in the physician's laboratory].

Lipid analysis should be tailored to the likelihood of hyperlipidemia and atherosclerosis. In healthy individuals without a family history of hyperlipidemia, it is sufficient to obtain readings of total cholesterol and high-density lipoprotein (HDL) cholesterol. In patients with a family history of hyperlipidemia, in addition, triglycerides should be measured. In patients with manifest atherosclerotic disease, the lipid profile should always include plasma cholesterol and triglycerides as well as HDL cholesterol; if these do not explain presence or extent of atherosclerosis, apolipoprotein (a) should be measured. Patients with diabetes mellitus should undergo the same diagnostic work-up as those with atherosclerotic disease. An apolipoprotein B reading (together with triglyceride levels) is sometimes helpful in patients with diabetes mellitus, allowing to estimate the size of triglyceride-rich lipoproteins. In patients with pancreatitis, longitudinal assessment of plasma triglycerides and, if available, measurement of HDL triglyceride are useful to unmask underlying hyperlipidemia.

Arteriosclerosis↗

Relation of cyclosporine blood levels to adverse effects on lipoproteins.

Hyperlipidemia is common in renal allograft recipients. To elucidate the role of cyclosporine in posttransplant hyperlipidemia, we measured lipids, lipoprotein lipids, and apolipoproteins of thirty-five renal allograft recipients and evaluated their relation to trough cyclosporine blood levels. All patients were on a triple immunosuppressive regimen with equal doses of prednisone and azathioprine, and had stable graft function. Cyclosporine blood levels were significantly correlated to total plasma cholesterol (P = 0.028), low-density lipoprotein cholesterol (P = 0.022), apolipoprotein B (P = 0.017), and the cholesterol/high-density lipoprotein cholesterol ratio (P < 0.002), but not to plasma triglycerides. Significant inverse correlations were found between cyclosporine blood levels and high-density lipoprotein cholesterol (P = 0.034), high-density lipoprotein3 cholesterol (P = 0.025), and apolipoprotein A-1 (P = 0.047), but not high-density lipoprotein2 cholesterol. The independent relation of cyclosporine blood levels to each of the measured lipid parameters was investigated by a stepwise regression model including age, body mass index, interval from transplantation, diabetes mellitus, plasma creatinine, and intake of diuretics and beta-blockers. After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. These data suggest that cyclosporine causes atherogenic dyslipidemia.

Adult↗

Fenofibrate improves postprandial chylomicron clearance in II B hyperlipoproteinemia.

In 11 patients with IIB hyperlipoproteinemia we studied fasting lipids, lipoproteins, lipoprotein-modifying enzymes, and postprandial lipid metabolism after a standardized oral fat load supplemented with vitamin A before and 12 weeks after treatment with fenofibrate, a third-generation fibric acid derivative. Fasting plasma cholesterol, triglycerides, low-density lipoprotein cholesterol decreased significantly (P < 0.05, P < 0.01, P < 0.01), high-density lipoprotein subfraction 3 cholesterol increased significantly (P < 0.05), and high-density lipoprotein subfraction 2 cholesterol remained unchanged. Postprandial lipemia, i.e., the integrated postprandial triglyceride concentrations corrected for the fasting triglyceride level, and postprandial chylomicron concentrations, as assessed by biosynthetic labeling of chylomicrons with retinyl palmitate, decreased by 40.6% and 60.1% (P < 0.05; P < 0.05), respectively. The activity of lipoprotein lipase (LPL) increased by 33.6% (P < 0.05); the increase in LPL during fenofibrate treatment was positively correlated with the increase in high-density lipoprotein cholesterol (r = 0.84; P < 0.005). Hepatic lipase and cholesteryl ester transfer protein mass and activity remained unchanged. We conclude that lipid-lowering therapy with fenofibrate ameliorates fasting and, more profoundly, postprandial lipoprotein transport in hypertriglyceridemia by curbing postprandial triglyceride and chylomicron accumulation, at least in part, through an increase in LPL activity.

Adult↗

Plasma triglycerides and three lipoprotein cholesterol fractions are independent predictors of the extent of coronary atherosclerosis.

BACKGROUND: The lipoprotein system has manifold links to atherosclerotic disease. LDL cholesterol is related to lesion formation and growth. The cholesterol of HDLs is indicative of protection against atherosclerosis. The status of triglycerides and of subfractions of high-density lipoproteins as risk factors is less certain. Also, the magnitude of the atherogenic/protective power of these factors is not known. METHODS AND RESULTS: Five hundred patients (418 men and 82 women) were enrolled in an angiographic study. A total of 1006 coronary lesions with > or = 50% narrowing were recorded as study end points. By extent of atherosclerosis, defined as the number of > or = 50% lesions, the study subjects were allocated to one of four ordered categories with 0, 1 to 3, 4 to 6, or 7 to 10 lesions, respectively. Subfractions of HDL cholesterol were determined by a dual precipitation method. By a polychotomous logistic regression model, it was found that, besides age and sex, LDL cholesterol, HDL2 cholesterol, HDL3 cholesterol, and triglycerides were independently predictive (P < .05) of the extent of coronary atherosclerosis. An increase in age by 10 years was associated with an increase of the odds ratio for falling into a higher-extent category by a factor of 1.64, and the same increase of the odds ratio was obtained by increasing LDL cholesterol by 0.92 mmol/L or triglycerides by 1.01 mmol/L and by decreasing HDL2 cholesterol by 0.20 mmol/L or HDL3 cholesterol by 0.46 mmol/L. The less sensitive coronary end point, presence of atherosclerosis (ie, observation of > or = 1 lesion of > or = 50%) depended significantly on age, sex, LDL cholesterol, and HDL2 cholesterol, but not on HDL3 cholesterol or triglycerides. CONCLUSIONS: In addition to LDL, HDL2, and HDL3 cholesterol, triglycerides also proved independently predictive of the extent of coronary atherosclerosis.

Cholesterol, HDL↗

[Low dosage intravenous calcitriol bolus therapy in chronic hemodialysis patients].

Severe secondary hyperparathyroidism in patients on chronic renal replacement therapy is still an immense problem, even after the introduction of the oral calcitriol therapy. Because the current first choice treatment--intravenous calcitriol-bolus application--fails to decrease parathyroidhormone (PTH) in some patients, we decided to monitor 22 chronic hemodialysis patients receiving low dose therapy with 3 x 1 micrograms calcitriol per week for a period of 6 months. After 6 months the PTH increased from 430 +/- 318 to 573 +/- 508 pg/ml (p < 0.05), the serum calcium from 2.14 +/- 0.22 to 2.31 +/- 15 mmol/l (p < 0.01). There was no significant change in serum phosphate, alkaline phosphatase (APH) and osteocalcin. The patients were divided into 2 groups according to their basal PTH-levels. Group 1 (n = 7, PTH < 200 pg/ml) showed a significant decrease of the PTH-levels from 99 +/- 38 to 61 +/- 53 pg/ml (p < 0.05). There was no significant change in serum calcium, phosphate, APH and osteocalcin levels. In group 2 (n = 15, PTH > 300 pg/ml) the PTH increased significantly (p < 0.05) from 585 +/- 287 to 812 +/- 439 pg/ml. No significant change was found for APH or osteocalcin. Calcium and phosphate levels increased significantly from 2.11 +/- 0.20 to 2.31 +/- 0.12 mmol/l (p < 0.01) and from 2.29 +/- 0.47 to 2.74 +/- 0.60 mmol/l (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Lipids and blood vessels].

The key lesion in atherosclerosis is termed atheroma. It consists of intracellular and extracellular cholesterol esters. Because atheromas are located subendothelially, an interrelation with blood cholesterol has long been suspected. In the blood, cholesterol is wrapped in lipoproteins, with the largest amount being found in low-density lipoproteins (LDL), whereas a smaller amount is found in high-density lipoproteins (HDL). LDL (and their cholesterol) are removed from the plasma by receptor-mediated uptake. Impaired LDL-receptor interaction results in accumulation of LDL in plasma. LDL now penetrate the endothelial layer and become deposited in the arterial intima. This process initiates atheroma formation. Excess tissue cholesterol (e.g. in the arterial intima) is returned to the liver by HDL. The HDL2 subfraction is particularly effective in this reverse cholesterol transport. Patients with coronary atherosclerosis either have a defect in reverse cholesterol transport (i.e. low HDL2 levels) or an excess in cholesterol load (i.e. high LDL). The ratio between LDL and HDL2 cholesterol determines the risk for atherosclerotic disease. Triglycerides lower HDL2 levels and thereby exert indirect atherogenicity.

Arteriosclerosis↗