Search PubMed⌕ Search

Biomedical subjects

H Schulz

Publications and source records attributed to H Schulz.

At least 325 records · Page 18Linked to original sources
PubMed1987

The interaction between EEG and transient muscle activity during sleep in humans.

The EEG and EMG were recorded during 14 nights of sleep for 5 young normal adults and were analyzed automatically with a lab computer system. From the EEG one parameter was computed which is based on the joint frequency-amplitude distribution of EEG waves. The temporal sequence of parameter values displays the time course of the sleep EEG. Another parameter, which results from the automatic analysis of the EMG, represents transient EMG activity, i.e. shortlasting changes of the muscle tone. A comparison of the automatically analyzed EEG and EMG data revealed a close correspondence between both parameters. A peak of EMG transient activity was observed in virtually each ultradian sleep cycle at a well-defined turning point between the phase of EEG synchronization and the subsequent phase of EEG desynchronization. Before and after this turning point there was a gradual decrease in the rate of transient EMG activity with minimal activity immediately preceding the turning point. The results suggest that cortical synchronization during sleep is incompatible with transient activity in the muscle system while desynchronization is invariably accompanied by a high rate of transient EMG activity.

Adult↗
PubMed1986

Channeling of 3-hydroxy-4-trans-decenoyl coenzyme A on the bifunctional beta-oxidation enzyme from rat liver peroxisomes and on the large subunit of the fatty acid oxidation complex from Escherichia coli.

Rates of the NAD+-dependent oxidation of 2-trans,4-trans-decadienoyl-CoA, a metabolite of trans-omega-6-unsaturated fatty acids, catalyzed by the mitochondrial enoyl-CoA hydratase plus 3-hydroxyacyl-CoA dehydrogenase and by the corresponding enzymes from peroxisomes, as well as Escherichia coli, were compared. The study of the mitochondrial system revealed that the conventional kinetic theory of coupled enzyme reactions cannot be applied to systems in which the primary reaction has a small equilibrium constant, and/or the concentration of coupling enzyme is higher than 0.01 Km for the intermediate and higher than the steady-state concentration of the intermediate. In contrast to the results obtained with the mitochondrial beta-oxidation system of unlinked enzymes, the steady-state velocities of 2-trans,4-trans-decadienoyl-CoA degradation catalyzed by either the peroxisomal bifunctional enzyme or by the E. coli fatty acid oxidation complex were found to be equal to the activities of enoyl-CoA hydratase even though the concentration of coupling enzyme was equal to that of the primary enzyme, and the quotient of Vmax/Km for the dehydration of 3-hydroxy-4-trans-decenoyl-CoA is much larger than the Vmax/Km for its dehydrogenation. The extraordinarily high efficiencies of these two multifunctional proteins in catalyzing the degradation of 2-trans,4-trans-decadienoyl-CoA is best explained by the direct transfer of the 3-hydroxy-4-trans-decenoyl-CoA intermediate from the active site of enoyl-CoA hydratase to that of 3-hydroxyacyl-CoA dehydrogenase. The discovery of an intermediate channeling mechanism on the peroxisomal bifunctional enzyme explains on the molecular level why the peroxisomal beta-oxidation system is well suited for the degradation of trans-fatty acids.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1986

3-Hydroxyacyl-CoA epimerases of rat liver peroxisomes and Escherichia coli function as auxiliary enzymes in the beta-oxidation of polyunsaturated fatty acids.

The beta-oxidation of 2-trans,4-cis-decadienoyl-CoA, an assumed metabolite of linoleic acid, by purified enzymes from mitochondria, peroxisomes, and Escherichia coli was studied. 2-trans,4-cis-Decadienoyl-CoA is an extremely poor substrate of the beta-oxidation system reconstituted from mitochondrial enzymes. The results of a kinetic evaluation lead to the conclusion that in mitochondria 2-trans,4-cis-decadienoyl-CoA is not directly beta-oxidized, but instead is reduced by NADPH-dependent 2,4-dienoyl-CoA reductase prior to its beta-oxidation. Hence, the mitochondrial beta-oxidation of 2-trans,4-cis-decadienoyl-CoA does not require 3-hydroxyacyl-CoA epimerase, a conclusion which agrees with the finding that 3-hydroxyacyl-CoA epimerase is absent from mitochondria (Chu, C.-H., and Schulz, H. (1985) FEBS Lett. 185, 129-134). However, 2-trans,4-cis-decadienoyl-CoA can be slowly oxidized by the bifunctional beta-oxidation enzyme from rat liver peroxisomes, as well as by the fatty acid oxidation complex from E. coli. The observed rates of 2-trans,4-cis-decadienoyl-CoA degradation by these two multi-functional proteins were significantly higher than the values calculated according to steady-state velocity equations derived for coupled enzyme reactions. This is attributed to the direct transfer of L-3-hydroxy-4-cis-decenoyl-CoA from the active site of enoyl-CoA hydratase to that of 3-hydroxyacyl-CoA dehydrogenase on the same protein molecule. All observations together lead to the suggestion that the chain shortening of 2-trans,4-cis-decadienoyl-CoA in peroxisomes and in E. coli occurs simultaneously by two different pathways. The major pathway involves the NADPH-dependent 2,4-dienoyl-CoA reductase, whereas 3-hydroxyacyl-CoA epimerase functions in the metabolism of D-3-hydroxyoctanoyl-CoA which is formed via the minor pathway.

Animals↗
PubMed1986

Rat heart fatty acid-binding protein is highly homologous to the murine adipocyte 422 protein and the P2 protein of peripheral nerve myelin.

The rat heart contains an abundant cytosolic protein which binds long chain fatty acids. We have determined its primary structure by Edman degradation of peptides generated from chymotryptic, tryptic, and elastase digestions. This polypeptide (Mr = 14,992) contains 134 amino acids and has a blocked (acetylated) NH2 terminus. The sequence of rat heart fatty acid-binding protein (FABP) is remarkably similar to the murine adipocyte 422 protein and the P2 protein of peripheral nerve myelin. Computer-assisted alignment of heart FABP and 422 revealed that 82 of 132 comparable residues are identical (62%). There are 77 identities out of 131 possible matches between this protein and the human myelin P2 protein (59%). Similar comparisons demonstrate that heart FABP has significant homology to several other proteins which bind hydrophobic ligands. The rank of order of similarity to heart FABP is: 422 greater than myelin P2 greater than cellular retinoic acid-binding protein greater than cellular retinol-binding protein II greater than cellular retinol-binding protein greater than intestinal FABP greater than liver FABP. These eight sequences form a family of paralogous homologues. Heart FABP has a region of internal homology involving tandemly arrayed oligopeptides spanning residues 71-100 and 101-131. This feature is not found in the 422 and P2 sequences. The endogenous ligands bound by the 422, P2, and heart FABP sequences have not been defined. Interpretation of the biological significance of their structural similarities and differences will require information about their ligand specificities and affinities.

Amino Acid Sequence↗
PubMed1986

Effect of growth hormone on fatty acid oxidation: growth hormone increases the activity of 2,4-dienoyl-CoA reductase in mitochondria.

The effect of growth hormone on the beta-oxidation of saturated and unsaturated fatty acids was studied with mitochondria isolated from control rats, hypophysectomized rats, and hypophysectomized rats treated with growth hormone. Rates of respiration supported by polyunsaturated fatty acylcarnitines, in contrast to rates observed with palmitoylcarnitine or oleoylcarnitine, were slightly lower in hypophysectomized rats than in normal rats, but were higher in hypophysectomized rats treated with growth hormone. The effects were most pronounced with docosahexaenoylcarnitine, the substrate with the highest degree of unsaturation. Since uncoupling of mitochondria with 2,4-dinitrophenol resulted in lower rates of docosahexaenoylcarnitine-supported respiration, while substitution of ATP for ADP yielded higher rates, it appears that energy is required for the effective oxidation of polyunsaturated fatty acids. Growth hormone treatment of hypophysectomized rats caused a threefold increase in the activity of 2,4-dienoyl-CoA reductase or 4-enoyl-CoA reductase (EC 1.3.1.34) in mitochondria, but not in peroxisomes. The activities of other beta-oxidation enzymes remained virtually unchanged. Rates of acetoacetate formation from linolenoylcarnitine, but not from palmitoylcarnitine, were stimulated by glutamate in mitochondria from hypophysectomized rats and hypophysectomized rats treated with growth hormone. All data together lead to the conclusion that the mitochondrial oxidation of highly polyunsaturated fatty acids is limited by the availability of NADPH and the activity of 2,4-dienoyl-CoA reductase which is induced by growth hormone treatment.

Acetoacetates↗
PubMed1986

[Determination of indole and skatole in seafood using high performance liquid chromatography (HPLC)].

A rapid and specific high-performance liquid chromatographic (HPLC) method for the determination of indole and 3-methylindole (skatole) is described. The detection limit of the two compounds is approx. 0.02 mg/kg. Gas chromatographic-mass spectrometric (GC-MS) confirmation of the identity has been carried out in shrimps. About 95% of added indole was recovered. The indole formation in shrimps, herring, and turbot, held under different storage conditions, is compared with other common quality indices such as TBA-value and alpha-tocopherol content.

Animals↗
PubMed1986

Studies on the tocopherol status in blood serum of premature babies and infants.

The level of naturally occurring tocopherols in blood serum of 88 preterm infants, aged from birth to 2 years, was determined by the high performance liquid chromatographic (HPLC) method using fluorescence detection. In 11 cases, patients were assayed for their tocopherol status in longitudinal studies, receiving known amounts of vitamin E supplements orally and/or parenterally. No correlation was found between serum alpha-tocopherol level and gestational age nor birth weight. All preterm infants receiving the vitamin E preparation showed an average serum tocopherol content of more than 0.5 mg/100 ml. The highest alpha-tocopherol concentration registered during vitamin E therapy was 3.28 mg/100 ml. Infusion of Intralipid, a product derived from fractionated soybean oil, caused a significant increase of gamma- and delta-tocopherol in blood serum. The half-life of delta-tocopherol in serum was calculated to be about 24 hours.

Administration, Oral↗
PubMed1986

Automatic analysis overcomes limitations of sleep stage scoring.

A computer programme for the automatic analysis of the sleep EEG and EMG is presented. An EEG parameter is derived which is based on the joint frequency-amplitude distribution of the EEG activity. This newly developed parameter stresses the dynamic development of sleep, composed of alternating phases of EEG synchronization and desynchronization. While synchronization develops slowly, the opposite phase of EEG activity, desynchronization, is more rapid. A particular advantage of the EEG parameter is its continuous scale which results in high resolution. Thus, the parameter reflects gradual EEG changes which a visual analyser would have to classify into the same sleep stage. In addition to the EEG, the EMG is analysed and two parameters are extracted, representing the mean muscle tone and transient EMG activation, respectively. There is a close temporal relationship between the EEG and the EMG with a maximum of transient EMG activity during the phase of EEG desynchronization. The properties of the automatic analysis were compared to the visual analysis on a sample of 12 all-night sleep records. The results show that the EEG parameter also agrees sufficiently with the traditional sleep scoring method and therefore is a valid descriptor of the time course of sleep.

Electroencephalography↗
PubMed1986

Anticonflict properties of the dipeptide Litoralon and of diazepam in rats.

The anticonflict properties of the anxiolytic diazepam and of the dipeptide Litoralon gamma-L-glutamyl-taurine and two of its analogues SZJ 3388, gamma-aminobutyryl-ethanolamine phosphate, and SZJ 3361, D-1-aminoisobutyrylethanolamine phosphate have been investigated in a "time-to-emerge" conflict paradigm in non-deprived rats. Diazepam, Litoralon and compound SZJ 3388 significantly decreased the "time-to-emerge" latency (TTE latency) in a dose-dependent manner versus saline- or vehicle-treated controls in doses between 0.05 and 0.50 mg/kg intraperitoneally. The analogue SZJ 3361 was inactive as regards the TTE latency, while the anti-histaminic promethazine lengthened the TTE latency in a dose-dependent manner. The number of irresolute responses was significantly decreased following administration of diazepam, SZJ 3388 and Litoralon and was positively correlated with the TEE latency-decreasing activity of these compounds. The data are discussed in terms of the benzodiazepine-like anxiolytic or anti-conflict properties of these dipeptides.

Animals↗
PubMed1986

[Topical use of prednicarbate preparations in children].

Prednicarbate (Dermatop) was topically applied in 50 children suffering from inflammatory dermatoses. In 12 children, the courses of therapy were documented by photographs. Its rapid onset of action, its lacking suppression of the endogenic biosynthesis of cortisol, as well as its small antiproliferative effect on cutaneous fibroblasts suggest that prednicarbate bears only minor risks especially for children's skin.

Administration, Topical↗
PubMed1986

[Photographic follow-up of the topical use of prednicarbate preparations in inflammatory dermatoses].

In 20 patients suffering from acute or chronic inflammatory dermatoses, topical treatment with prednicarbate (Dermatop) was photographically documented and evaluated. Because of the rapid and pronounced anti-inflammatory and anti-edematous effect of prednisolone-17-ethyl carbonic ester without halogenic groups, therapy took only 7 to 21 days. Since there was practically no suppression of the endogenic biosynthesis of cortisol and no atrophogenic potency, we expected a minimum of side effects along with a maximum of therapeutic results.

Administration, Topical↗