Biomedical subjects
Publications and source records attributed to R Müller.
4-Chlorobenzoate dehalogenase from Pseudomonas sp. strain CBS3 converted 4-chloro-3,5-dinitrobenzoate to 3,5-dinitro-4-hydroxybenzoate and 1-chloro-2,4-dinitrobenzene to 2,4-dinitrophenol. The activities were 0.13 mU/mg of protein for 4-chloro-3,5-dinitrobenzoate and 0.16 mU/mg of protein for 1-chloro-2,4-dinitrobenzene compared with 0.5 mU/mg of protein for 4-chlorobenzoate.
In extracts from Arthrobacter sp. SU DSM 20407 an enzyme was detectable, that converted 4-chlorobenzoate into 4-hydroxybenzoate. This conversion was also observed when no oxygen was present in the reaction mixture. Boiling for 5 min destroyed the enzyme activity. 4-Bromo- and 4-iodobenzoate were substrates for the enzyme too, but not 4-fluorobenzoate, 4-chlorophenylacetate and 4-chlorocinnamic acid. The enzyme showed optimum activity at 16 degrees C and at pH 7-7.5. The specific activity in the extracts varied between 0.5 and 5 mU/mg of protein. Zn2+ and Cu2+ inhibited the enzyme, while H2O2 slightly activated. In contrast to all other 4-chlorobenzoate dehalogenases described before the enzyme was not inhibited by EDTA, nor was it activated by Mn2+. Other divalent ions also had no effect. The molecular mass of the enzyme was 45,000 +/- 5,000 Da as judged by gel-filtration.
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Nine cardiac patients treated with digitalis participated in a 3-week study with the aim to investigate whether digoxin (beta-acetyldigoxin) interacts with the new 1,4-benzodiazepine metaclazepam. Comparison of the plasma digoxin levels under placebo and metaclazepam treatment showed no statistically significant differences, i.e. no interactions between digoxin and metaclazepam were found.
To assess the role of atrial natriuretic peptide (ANP) in relation to the sympathoadrenal and renin-angiotensin-aldosterone system, and sodium excretion, 88 cirrhotic patients (mean age 52 years; 28 compensated, 28 decompensated with ascites, and 32 decompensated and treated with diuretics) and 26 control subjects were investigated. Basal ANP levels were not different between any group of cirrhotics and controls. Circulating ANP was not related to elevated plasma noradrenaline and adrenaline, and enhanced plasma renin/aldosterone levels in ascitic patients. Furthermore, ANP was not related to urinary sodium excretion, blood pressure, and heart rate. In 30 cirrhotic patients (12 compensated, 18 decompensated with ascites including eight on diuretic therapy) and nine controls, a passive leg rising procedure for 1 h was performed in order to augment central blood volume and atrial pressure physiologically. Ascitic patients (with and without diuretic treatment) experienced a slight but significant increase in plasma ANP indicating preserved responsiveness of ANP release in cirrhosis. Plasma aldosterone was markedly depressed. The data support the underfilling concept of ascitic formation in advanced stages of cirrhosis. The failure of enhanced ANP release under basal conditions may be due to the diminished effective blood volume, resulting in insufficient atrial stretching.
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The amplitudes of the motion VEP waves P100, N200 and P300 were investigated on 12 subjects at six electrode positions (2.5, 5, 7.5 and 10 cm above the inion and 5 cm bilaterally from the 2.5 cm midline point). The evaluation was performed on the basis of in general 45 (for P100 32) averaged potentials per subject. Each averaged potential was obtained from 40 single potentials. P100: The amplitudes were nearly equal at all electrodes. N200: The greatest amplitudes could be found at the lateral electrodes. The amplitudes decreased in the midline in occipito-frontal direction reaching the lowest value at the electrode most frontally situated. P300: This wave had its greatest amplitude at the most frontal lead position. The amplitude decreased systematically in occipital direction. The differences in the position of the amplitude maxima and in the topographical distribution of the remaining amplitude values suggest different generator structures of the waves N200 and P300.
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A cortical potential was evoked by the onset of horizontal drift of a previously stationary vertical square-wave grating (motion-on VEP). The influence of contrast on the principal VEP waves N2 and P2 (peak latencies 180-220 ms and 250-350 ms, respectively) was investigated in five subjects for velocities between 0.3 and 4.1 deg/s, a spatial frequency of 2.6 c/deg and a mean luminance of 17 cd/m2. For low contrasts an ascending linear relation could be found between wave amplitude and logarithm of contrast, and a descending one between wave peak latency and log contrast. The waves remained constant for moderate and high contrasts. The lowest contrast value at which wave constancy occurred (saturation contrast) was determined by a method of least squares. All the data summarized yielded a saturation contrast of 0.058 for N2 and 0.084 for P2. The saturation contrast of the pattern VEP already known from the literature is essentially greater under comparable experimental conditions.
The cortical potential visually evoked by motion of a periodic grating (motion VEP) is composed of a transient component which decays within 500 ms of stimulus-onset (motion-on VEP) and a sustained component. Amplitude and peak latency of wave N2 of the motion-on VEP are functions of grating velocity. Both remain constant at spatial frequencies between 0.6 and 4.3 c/deg and at temporal frequencies within the equivalent intervals. The transient component of the motion VEP is independent of the spatial phase position of the grating before motion onset. The sustained component can only be seen in the averaged motion VEP at constant phase position of the grating before motion onset. This potential consists of periodical fluctuations with a main frequency equal to the temporal frequency of the moving grating. As a result of psychophysical investigations some authors suggest pattern velocity is the relevant variable of velocity perception, others temporal frequency. The motion VEP is dependent on both velocity and temporal frequency, the transient component is a function of velocity, the sustained component of temporal frequency.
The purpose of this study was to measure left-ventricular end-diastolic pressure (LVEDP) noninvasively by pulsed Doppler ultrasound. In 30 consecutive patients of mean age 57.4 +/- 10.2 years (range 32 to 72 years) undergoing left-heart catheterization for exclusively diagnostic reasons LVEDP (range 5 to 33 mm Hg, mean 14.8 +/- 0.61 mm Hg) was measured invasively. Immediately before cardiac catheterization the flow profile along the mitral valve was derived by pulsed Doppler ultrasound. The typical flow profiles characterizing the early diastolic passive (e-wave) and late diastolic active by atrial contraction caused inflow (l-wave) into the left ventricle and represented the indexes of left ventricular diastolic function. The ratio of the velocity-time-integrals in early (e) and late diastole (l) corresponds to the ratio of blood flow along the mitral valve in early and late diastole. It could be shown that there is a highly significant linear correlation (r = 0.98, p less than 0.001) between the ratio of the velocity-time-integrals of late to early diastole (l/e-ratio) and LVEDP. LVEDP can be calculated by means of the l/e-ratio according to the formula: LVEDP (in mm Hg) = 15.15 X l/e-ratio + 1.06 With increasing LVEDP the proportional share of the active mitral blood flow in the diastole increased; the share of the early diastolic passive blood flow decreased proportionally. In patients with a l/e-ratio greater than 1.2 LVEDP, was always greater than 18.5 mm Hg; in patients with l/e-ratio greater than 0.9, LVEDP did not exceed 15 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
Haemorheological knowledge achieved in the past decade has revealed the essential interactions of flow properties of blood with haemostatic, coagulation, and vessel wall mechanisms in blood flow disturbances. Fine tuning of these factors maintains the physiologically adequate perfusion of the nutritive microcirculation. Under pathological conditions, therefore, the most beneficial effect can be expected from the therapeutic approaches which, apart from the disturbed flow properties of the blood itself, improve also all the other factors involved. In consequence, it is suggested that treatment of circulatory disturbances should be directed not only at the reduction of enhanced red blood cell aggregation and improvement of impaired red blood cell deformability, but also at a diminuation of enhanced platelet and white cell hyperreactivity as well as at an amendment of hypercoagulability and of the affected endothelial and vessel wall systems. Experimental and clinical studies are reviewed to show that pentoxifylline meets these different requirements to a great extent. Its multi-functional pharmacological profile suggests new aspects in the treatment of circulatory disorders in many diseases and in the prevention of thrombotic events.