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H Schulz

Publications and source records attributed to H Schulz.

At least 361 records · Page 20Linked to original sources
PubMed1983

Metabolism of 4-pentenoic acid and inhibition of thiolase by metabolites of 4-pentenoic acid.

The metabolism of 4-pentenoic acid, a hypoglycemic agent and inhibitor of fatty acid oxidation, has been studied in rat heart mitochondria. Confirmed was the conversion of 4-pentenoic acid to 2,4-pentadienoyl coenzyme A (CoA), which either is directly degraded via beta-oxidation or is first reduced in a NADPH-dependent reaction before it is further degraded by beta-oxidation. At pH 6.9, the NADPH-dependent reduction of 2,4-pentadienoyl-CoA proceeds 10 times faster than its degradation by beta-oxidation. At pH 7.8, this ratio is only 2 to 1. The direct beta-oxidation of 2,4-pentadienoyl-CoA leads to the formation of 3-keto-4-pentenoyl-CoA, which is highly reactive and spontaneously converts to another 3-ketoacyl-CoA derivative (compound X). 3-Keto-4-pentenoyl-CoA is a poor substrate of 3-ketoacyl-CoA thiolase (EC 2.3..1.16) whereas compound X is not measurably acted upon by this enzyme. The effects of several metabolites of 4-pentenoic acid on the activity of 3-ketoacyl-CoA thiolase were studied. 3,4-Pentadienoyl-CoA is a weak inhibitor of this enzyme that is protected against the inhibition by acetoacetyl-CoA. The most effective inhibitor of 3-ketoacyl-CoA thiolase was found to be 3-keto-4-pentenoyl-CoA, which inhibits the enzyme in both a reversible and irreversible manner. The reversible inhibition is possibly a consequence of the inhibitor being a poor substrate of 3-ketoacyl-CoA thiolase. It is concluded that 4-pentenoic acid is metabolized in mitochondria by two pathways. The minor yields 3-keto-4-pentenoyl-CoA, which acts both as a reversible and as a irreversible inhibitor of 3-ketoacyl-CoA thiolase and consequently of fatty acid oxidation.

Acetyl-CoA C-Acetyltransferase↗
PubMed1983

Multienzyme complexes of fatty acid oxidation from Escherichia coli K12 and from a mutant with a defective L-3-hydroxyacyl coenzyme A dehydrogenase.

An Escherichia coli mutant (fadB64), with a defective L-3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35) which is unable to grow on long-chain fatty acids as the sole carbon source, was shown to possess a fatty acid oxidation complex that contains five beta-oxidation enzymes, including L-3-hydroxyacyl-CoA dehydrogenase. A comparative study of the complexes from the mutant, from its parental strain and from wild-type E. coli B demonstrated the immunological and gross structural identity of all three fatty acid oxidation complexes. A kinetic evaluation of the complexes led to the suggestion that the mutation may have affected the active site of L-3-hydroxyacyl-CoA dehydrogenase so that it is inactive with acetoacetyl-CoA as a substrate, but exhibits an increasing percentage of the parental dehydrogenase activity with increasing chain length of the substrate.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1983

A quantitative determination of anticonvulsant-induced bone demineralization by an improved X-ray densitometry technique.

Quantitative studies of the influence of anticonvulsant drugs on bone mineral content of 88 epileptics were performed by a microcomputer-aided densitometer system. The results showed that the mineral content decreases significantly with the duration of the therapy. This decrease was found to be approximately 1.2% per year for a Diphenylhydantoin (DPH) monotherapy and 1.8% per year and 2.0% per year for a DPH plus Phenobarbital and DPH plus Carbamazepin combination therapy.

Absorptiometry, Photon↗
PubMed1983

REM latency: development in the first year of life.

The development of REM latency in the first year of life was investigated in two groups of 10 infants each. While 10 infants were normal, the other 10 underwent continuous feeding for various gastrointestinal diseases. Each infant was continuously recorded polygraphically for 24 h. While younger infants (less than or equal to 3 months) manifested predominantly shorter REM latencies (less than or equal to 8 min), older infants (4-13 months) produced a mixed distribution of short and long REM latencies. The total distribution of the REM latencies appears to be bimodal with latencies either shorter than 8 min or longer than 16 min. It is only in the group of older infants that the temporal distribution of REM latencies constitutes a diurnal rhythm, with the longest latencies in the interval between 12:00 and 16:00 and the shortest between 4:00 and 8:00. In the group of older infants, REM latency also depends on the duration of prior wakefulness. Long REM latencies are significantly more often preceded by long episodes of wakefulness than are short REM latencies. The different feeding conditions had only a minor effect on REM latency.

Humans↗
PubMed1983

Rate and distribution of body movements during sleep in humans.

Body movements were measured during sleep with a mechanoelectrical transducer in 11 healthy adults. Also measured were the electroencephalogram (EEG), electrooculogram (EOG), and electromyogram (EMG). Each subject slept alone in a quiet room for 21 to 44 consecutive nights. Body movements were classified as minor movements (actogram signal or head leads artifact), major movements (actogram signal plus head leads artifact), or movement time (MT). There was a strong relationship between rate of body movements and sleep stages, with the rate decreasing along the following sequence of stages: W greater than S1 greater than REM greater than S2 greater than S (3 + 4). If the body movements for all nights are pooled per subject, the distribution of body movement rates shows hardly any overlap for the Stages 1, REM, 2, and (3 + 4). The relative frequency of body movements seems to be regulated by a stage-dependent mechanism. The reliability of the body movement rate was determined by computing correlations between pairs of adjacent nights, which resulted in a rtt = .69. When 2 to 9 nights were pooled stepwise according to a split-half procedure, the mean rtt increased and reached values between .80 and .90, which means that body movements are a reliable sleep measure especially if the time base is large enough.

Adult↗
PubMed1983

Sleep onset REM episodes are associated with circadian parameters of body temperature. A study in depressed patients and normal controls.

Sleep and 24-hr body core temperature were measured during a 2- to 3-week study interval in 15 endogenous depressives, 12 patients after remission, and 10 normal control subjects. The total sample was subdivided into one group of persons who displayed at least one sleep onset REM episode (SOREM; latency less than or equal to 20 min) during the study interval and another group of persons who never had SOREMs; 14 persons (8 depressives, 3 remitted patients, and 3 control subjects) belong to the SOREM group, 23 persons (7 depressives, 9 remitted patients, and 7 control subjects) to the group without SOREMs. While the groups do not differ in the mean body core temperature, members of the SOREM group have a significantly smaller variation around the daily mean value. This is mainly due to a smaller difference between daytime and nighttime body temperature in the SOREM group. These data suggest that short REM latency is closely associated with alterations of body core temperature.

Body Temperature↗
PubMed1982

Evidence for a modified pathway of linoleate degradation. Metabolism of 2,4-decadienoyl coenzyme A.

The enzymatic degradation of 2,4-decadienoyl-CoA, an assumed metabolite of linoleic acid, was studied in vitro. 2-trans,4-trans-Decadienoyl-CoA, a metabolite of unsaturated fatty acids with trans double bonds, was readily degraded by a beta-oxidation system reconstituted from purified enzymes, as well as by rat heart mitochondria. In contrast, a mixture of 2-cis,4-cis-decadienoyl-CoA and 2-trans,4-cis-decadienoyl-CoA, the latter of which is assumed to be a metabolite of linoleic acid, was acted upon neither by the reconstituted beta-oxidation system nor by the beta-oxidation system present in rat heart mitochondria. However, all three 2,4-decadienoyl-CoA isomers were rapidly reduced by the NADPH-dependent 2,4-dienoyl-CoA reductase of rat heart mitochondria. Based on these observations, we conclude that 2-trans,4-cis-decadienoyl-CoA, a metabolite of linoleic acid, is not directly degraded via the beta-oxidation cycle, but instead is reduced by the NADPH-dependent 2,4-dienoyl-CoA reductase to 3-decenoyl-CoA which is further degraded via the beta-oxidation pathway.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1982

[Identification of the site of block in high degree AV conduction disorders on the surface ECG].

The possibility of identifying the site of block by analysing the surface ECG was studied in 124 patients with 2nd or 3rd degree AV-block. In all cases His-bundle-electrography was performed. With regard to the QRS-duration (both in conducted and in escape beats) and to functional peculiarities of the AV-conduction or of the automatic centres in patients with narrow QRS complexes nearly all cases with the prognostically less favourable His-Purkinje-block are discernible.

Bundle of His↗
PubMed1982

4-Bromocrotonic acid, an effective inhibitor of fatty acid oxidation and ketone body degradation in rat heart mitochondria. On the rate-determining step of beta-oxidation and ketone body degradation in heart.

4-Bromocrotonic acid was found to effectively inhibit respiration supported by either palmitoylcarnitine or acetoacetate in coupled rat heart mitochondria. Partial inhibition was observed when 3-hydroxybutyrate served as a substrate, whereas pyruvate-supported respiration was unaffected by the inhibitor. Thus, 4-bromocrotonic acid inhibits fatty acid oxidation and ketone body degradation. When the enzymes of beta-oxidation and ketone body degradation were assayed in mitochondria preincubated with 4-bromocrotonic acid, only 3-ketoacyl-CoA thiolase and acetoacetyl-CoA thiolase were found to be inactive. Evidence is presented for the enzymatic conversion of 4-bromocrotonic acid to 3-keto-4-bromobutyryl-CoA which effectively inhibits both thiolases. A kinetic evaluation of the inhibitions caused by 4-bromocrotonic acid in coupled rat heart mitochondria demonstrated that 3-ketoacyl-CoA thiolase and respiration supported by palmitoyl carnitine are inactivated at equal rates. However, acetoacetyl-CoA thiolase was inactivated more rapidly than was respiration supported by acetoacetate. It is suggested that the thiolase-catalyzed step is rate-limiting in beta-oxidation or is as slow as other reactions are. In contrast the thiolytic cleavage of acetoacetyl-CoA does not seem to be rate-limiting in ketone body degradation.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1982

[Thyroid hormones in metastasizing prostate cancer treated with polyestradiol phosphate].

Patients with prostate cancer demonstrate a significant change in thyroid hormones when treated with estrogens after orchiectomy. Low-dose estrogen treatment for more than six months stimulates the synthesis of thyroxine-binding globulin. As a consequence, serum level of thyroxine is also increased. Serum free thyroxine is distinctly lowered by estrogen treatment while the linear ratio of thyroxine and free thyroxine is disturbed.

Aged↗
PubMed1982

[Fungal infections in urologic diseases with special reference to mixed bacterial infection].

A report is given on the mycological examination of urine from 146 urological patients. The possible influence of a mixed infection with bacteria on the growth of blastomyces is discussed. Whereas in the organism bacteria and blastomyces can exist well in conjunction, especially gram-negative bacteria in a culture medium can inhibit the growth of blastomyces. The result would be wrongly negative culture results. In our tests mixed infections of candida albicans and/or candida guilliermondii with escherichia coli and/or enterococci were found. Therefore it is recommended to add a suitable antibacterial antibiotic to the test material and to carry out a simultaneous bacterial urine culture. Where there is a urological primary disease and the urine has to be sent a long way we recommend Gentamycin, in a dosage of 200 micrograms/ml urine, for its good sensitivity.

Aged↗
PubMed1982

[Synthesis and enzymatic degradation of beta-casomorphin-5 (author's transl)].

The authors describe the synthesis of beta-casomorphine-5 (Tyr-Pro-Phe-Pro-Gly) by segment condensation and stepwise building-up. Intracerebroventricular application of the pentapeptide to the rat produces a long-lasting analgesia against thermal stimuli (which can be inhibited by naloxone) and counteracts the extinction of a passive avoidance reaction for no less than 4 days following post-shock application. beta-Casomorphin-5 is very rapidly degraded by dipeptidylpeptidase IV; the degradation starts from the N-terminus giving dipeptides. The degradation products are competitive inhibitors of this enzyme.

Analgesics↗
PubMed1982

Distribution of REM latencies after sleep interruption in depressive patients and control subjects.

The REM sleep latency of 16 endogenous depressives and 10 normal controls was obtained over a series of nights, once at evening onset of sleep and once after a deliberate sleep interruption at 2:30 AM. Twelve of the patients were studied again during a follow-up some months later, when they were free of depressive symptoms. The patients were classified into Group A (n = 9) if they displayed sleep onset REM episodes (SOREMs) at evening sleep onset, or Group B if they did not have SOREMs at evening sleep onset. Group A patients had significantly more SOREMs after the deliberate sleep interruption than Group B patients, during depression as well as in the symptom-free interval. REM latency appears to depend on several different factors: (a) the predisposition of the person, (b) the time of day, and (c) REM pressure, which seems to increase within a REM-REM interval.

Adult↗
PubMed1981

[What is illness?].

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Attitude to Health↗