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Biomedical subjects

R Engler

Publications and source records attributed to R Engler.

At least 73 records · Page 4Linked to original sources
PubMed1982

[Increased activity of adenine phosphoribosyl transferase in a child trisomic for 16q22.2 to 16qter due to malsegregation of a t(16;21) (q22.2;q22;2)pat (author's transl)].

Two cousins with trisomy for the distal third of 16q due to a familial translocation, t(16;21)(q22.2;q22-2), are reported. The APRT gene locus could be assigned to 16q22.2 to 16qter. The phenotypic similarities of the first patient, who had trisomy 16q22.3 to 16qter and monosomy 21q22.3, to six other patients with partial trisomy 16q reported in literature allows the delineation of a syndrome due to trisomy 16qter. In the second patient, with trisomy 16q22.3 to 16qter and trisomy 21pter to 21q22.2 similar features are present but in association with the classical symptoms of trisomy 21.

Adenine Phosphoribosyltransferase↗
PubMed1981

A new pentraxin (serum amyloid P-component) in the rat: evidence for two quaternary structures and effect of ligands on self-association.

A new rat serum protein has been isolated by affinity chromatography using ethanolamine- or phosphoethanolamine-substituted agarose gels. This protein has the morphological and functional characteristics of serum amyloid P-component and C-reactive protein. It comprises C5 cyclic symmetry structure with non covalently cross-linked subunits which have calcium-dependent binding sites. We have called this protein rat serum amyloid P-component since it has all the properties typical of human serum amyloid P-component: it is made up to 10 subunits, it contains sialic acid and hexoses, it forms macroscopic polymers and its does not precipitate with pneumococcal C-polysaccharide. Rat amyloid P-component has three remarkable properties. Electron microscopy has shown that apart from pentagonal figures and stacked discs, rat P-component has a C10 cyclic symmetry structure. Rat amyloid P-component has an affinity for specific ligands, such as phosphorylcholine or phosphoethanolamine. These ligands are able to depolymerize self-associated rat P-component. With these characteristics, rat serum amyloid P-component could prove to be an important model in the study of the relations between amyloid P-component and amyloidosis.

Amyloid↗
PubMed1981

[Decreased binding by isolated rat hepatocytes of asialo-haptoglobin after combination with hemoglobin].

The desialilation of 125I-labelled haptoglobin unmasks non-reducing galactose which has become terminal and permits its recognition and binding by isolated hepatocytes. However, the prior formation of an asialohaptoglobin-haemoglobin complex diminishes this property considerably. The explanation suggested is that there could either be a structural rearrangement of the complexed asialo-haptoglobin or steiric hindrance due to a masking of the galactose by the haemoglobin.

Animals↗
PubMed1981

Patient activated asynchronous ventricular pacing at normal rates for termination of ventricular tachycardia.

Ventricular pacing has been used to prevent or convert ventricular tachycardia. We report the use of patient-activated asynchronous mode ventricular pacing at normal rates for conversion of ventricular tachycardia by competitive pacing impulses. Following electrophysiologic studies, a specially constructed pacemaker was inserted. Routine function mode resulted in no output but activation of the reed switch resulted in V00 (asynchronous) pacing at 80/min. Patient-initiated conversion of ventricular tachycardia was documented by ambulatory electrocardiographic monitoring. The patient reports an average of two episodes per month converted over a four year period.

Cardiac Pacing, Artificial↗
PubMed1981

[Hemolysis and plasma proteins (author's transl)].

Simultaneous assay of haptoglobulin, hemopexin and orosomucoid allowed detection and quantification of intravascular hemolysis with or without inflammatory reactions. In cases of intravascular or extravascular hemolysis, the concentration of plasma haptoglobulin is greatly diminished, this generally being accompanied by an increase in free bilirubin. This last characteristic allows differentiation from intravascular hemolysis where the free bilirubin concentration remain normal.

Blood Proteins↗
PubMed1980

Kinetic study of the interaction between rat haptoglobin and rat liver cathepsin B.

One of the roles of the acute phase reactants (APR), according to Koj, is to regulate the action of tissue proteinases released during the inflammatory reaction. To study this phenomenon in vitro, rat liver cathepsin B (EC 3.4.22.1), a lysosomal proteinase, and a typical APR, rat serum haptoglobin, were purified. By kinetic study, haptoglobin was found to inhibit cathepsin B and the inhibitory activity of a competitive type was increased with the molecular weight of the substrate. When 125I-labelled denatured bovine serum albumin (BSA) was used as a substrate, the apparent Michaelis constant (Km app.) for cathepsin B was 5 +/- 0.4 X 10(-6) M. When haptoglobin was added, the apparent inhibition constant (Ki app.) was 3.5 +/- 1.5 X 10(-8) M. Native haptoglobin was not catabolized by cathepsin B while under the same conditions denatured haptoglobin was degraded by the enzyme.

Animals↗
PubMed1979

Is immunochemical determination of haptoglobin phenotype dependent?

Immunochemical methods have been used to determine the concentration of haptoglobins. The dependence on the phenotype was tested with highly purified Hp 2-1, Hp 2-2 and Hp 1-1, by immunonephelometry and radial immunodiffusion (RID). Measurements with three different instruments: automated immunonephelometer (AIP, Technicon), laser nephelometer (LN, Behring) and immunochemistry system (ICS, Beckman) were performed. For each type of apparatus antisera against a pool of haptoglobins were provided by the respective manufacturers. Some experiments were done with an antiserum to the haptoglobin heavy chain prepared in the laboratory. This study shows that haptoglobin determination depends neither on the physical geometry of the instruments or on the type of antiserum used in this work. In contrast, the data display a dependence on haptoglobin phenotype. When Hp 2-1, the most common phenotype, is taken as a standard, thd values obtained for Hp 2-2 are in good agreement with those obtained for Hp 2-1. However, the values obtained for Hp 1-1 are overestimated unless they are corrected by an experimental factor which has been determined in this study.

Haptoglobins↗
PubMed1979

Efficacy of a new oral agent (tocainide) in the acute treatment of refractory ventricular arrhythmias.

To assess the efficacy of tocainide, a new oral analog of lidocaine, 30 patients with ventricular arrhythmias refractory to quinidine, procainamide and propranolol were treated with this agent. The dose of tocainide ranged from 400 to 800 mg every 8 hours. Peak tocainide blood levels 1 to 4 hours after administration ranged from 5.0 to 15.0 microgram/ml (mean 10.3). The suppression of ventricular premature beats by 75 percent or more was arbitrarily used as a measure of drug efficacy. In 13 patients who met this criterion, ventricular premature complexes, assessed with 24 hour ambulatory tape monitoring, decreased by an average of 88 percent. In 8 of 11 patients, repeated symptomatic bouts of ventricular tachycardia were completely suppressed. Considering both the response of ventricular premature complexes and the abolition of ventricular tachycardia, 18 patients (60 percent) responded to tocainide. Twenty-one patients (70 percent) had initial gastrointestinal and central nervous system side effects; most of these were transient or responded to a reduction in dose. In two patients disorientation and a skin rash required withdrawal of tocainide. These adverse effects did not appear to be due to the interaction of tocainide with other antiarrhythmic agents. It is concluded that tocainide is an effective oral agent for the therapy of potentially lethal ventricular arrhythmias refractory to other medication.

Administration, Oral↗
PubMed1979

[Preparation and seric form of rabbit C reactive protein].

The preparation of rabbit C-reactive protein (CRP) involves a single step affinity chromatography. This preparation takes advantage of the calcium-dependent affinity of CRP for an agarose gel bearing 2-aminoethanol dihydrogen-phosphate as a ligand. A prior chromatography on agarose gel without the ligand allows the uptake of the serum amyloid P-component (SAP). The CRP prepared according to this method is able to form precipitating complexes in agarose with rabbit lipoproteins. The specificity of these interactions is studied. It is demonstrated that CRP-High Density Lipoproteins (HLD) association produces a second precipitation arc when the pure CRP is revealed by a specific antiserum in agarose. Moreover, CRP in the serum is shown to be in the bound form only, and the binding involves Low Density Lipoproteins (LDL) exclusively.

Animals↗
PubMed1977

Platelet aggregate ratios--standardization of technique and test results in patients with myocardial ischemia and patients with cerebrovascular disease.

The technique for measuring platelet aggregate ratios described by Wu and Hoak (1974) was evaluated in normal subjects. The following had no influence upon the test result: age, sex, fasting versu the postprandial state, and the degree of stasis prior to drawing the sample. Variance within subjects was small compared to variance between subjects (0.009 versus 0.0053, p less than 0.01). Platelet aggregate ratios were then measured in 36 patients with coronary artery disease hospitalized with acute chest pain. Their mean platelet aggregate ratio of 0.86 was identical to the mean ratio for 47 normal subjects. Greater variability was found within patients (between samples) than within the normal subjects. This observation raises doubts about the significance of a single measurement of platelet aggregate ratio in such acutely ill patients. Mean platelet aggregate ratios measured daily did not differ over a 7-day period between 11 patients who developed a myocardial infarction and 10 patients who did not. A normal mean platelet ratio was also found on a single measurement from 30 patients with a history of completed stroke (0.87) and from 11 patients with a history of transient ischemic attacks (0.92).

Adult↗