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Biomedical subjects

L Schmidt

Publications and source records attributed to L Schmidt.

At least 145 records · Page 8Linked to original sources
PubMed1986

A prospective study of inhibitive casting as an adjunct to physiotherapy for cerebral-palsied children.

The effect of a three-week course of inhibitive casting and neurodevelopmental therapy on the static muscle tonus, developmental skills, passive range of ankle dorsiflexion and gait pattern was determined in 32 cerebral-palsied children. Two weeks after treatment, passive range of ankle dorsiflexion and foot-floor contact in walking had improved significantly but there was no significant change in the static muscle tone or developmental skills. After five months the improvements in ankle dorsiflexion and walking pattern were no longer evident. Further objective studies to determine the effect of 'inhibitive casting' are necessary before the modality is used indiscriminately.

Ankle↗
PubMed1986

Current problems of the diagnostics of the retroperitoneum.

The authors discussed the examinations yielding optimal results in revealing the pathological retroperitoneal processes. Among those were bilateral dorsopedal lymphography, ultrasonography and computed tomography. They evaluated these examinations in detecting the retroperitoneal lymph node metastases of 15 non-seminoma patients. They describe their 4 cases of extragonadal germ-cell and testicular tumours and speculate on their development. They suppose that the 'unexplainable' renal colics of the older male patients can possibly be due to primary retroperitoneal germ-cell tumours.

Aged↗
PubMed1985

Combined thin layer chromatography/mass spectrometry: an application of 252Cf plasma desorption mass spectrometry for drug monitoring.

The pharmacokinetic analysis is performed in a three-step procedure: sample extraction, sample purification by thin layer chromatography (TLC) and quantitative sample detection by time-of-flight (TOF) mass spectrometry. 252Cf plasma desorption (PD) mass spectrometry utilizing the fission fragment-induced ionization and desorption of non-volatile compounds is suitable as a universal, non-destructive detector in TLC. Here TLC and mass spectrometry are operated in an off-line combination. As an example some pharmacokinetic data for etoposide (VP 16-213) together with calibration data are presented. The new experimental method is discussed in terms of sensitivity and detection limit.

Californium↗
PubMed1985

Drug monitoring of etoposide (VP16-213). I. A combined method of liquid chromatography and mass spectrometry.

Drug monitoring is performed by means of sample extraction, sample purification by high-performance liquid chromatography (HPLC), and sample detection by time-of-flight mass spectrometry. This mass spectrometry utilizing 252Cf fission fragment-induced ionization and desorption of nonvolatile compounds is suitable as a universal, nondestructive detector in HPLC. Liquid chromatography and mass spectrometry are combined, so that mass analysis can be operated online and offline to the fractional sampling of the effluent and the samples can still be recovered. As an alternative to HPLC separation, samples can be purified by thin-layer chromatography (TLC), resulting an offline TLC + MS combination. Preliminary pharmacokinetic data for etoposide (VP16-213) together with calibration data are presented, and are discussed with reference to the sensitivity and detection limit of the new experimental method.

Californium↗
PubMed1985

Increased excretion of harman by alcoholics depends on events of their life history and the state of the liver.

Based on the hypothesis of a relationship between the concentration of trace amines like tetrahydroisoquinolines (TIQ's) and beta-carbolines (BC's) in the brain and an increased voluntary ingestion of ethanol, the concentrations of ethanol, acetaldehyde and harman (a beta-carboline) were examined in a group of 20 alcoholics. The patients excreted a higher amount of harman into the urine than non-alcoholics on the day of admission (harman-1) as well as at the end of the detoxication period, 14 days later (harman-14). Certain factors were related to the increased excretion of harman by alcoholics: The younger the patient when he/she consumed ethanol for the first time, the higher the concentration of acetaldehyde in the blood and the amount of harman (harman-14) excreted in the urine. Furthermore, the younger the patient when he/she was intoxicated with ethanol for the first time the higher the amount of harman (harman-14) in the urine. Patients with first grade relatives who were alcoholics excreted more harman (harman-14) than those without such relatives. The following variables were not related to harman-14: The average amount of ethanol consumed daily during the 6 months prior to admission, the presence of signs of intoxication and symptoms of withdrawal at admission to hospital, and the consumption of other psychotropic substances. A negative correlation was found between the state of the liver, as assessed by liver histology and gamma-glutamate transferase (gamma-GT) levels, and the concentration of harman in the urine. Thus, some events in the patient's history as well as the state of the liver are important for the increased excretion of harman into urine of alcoholics.

Acetaldehyde↗
PubMed1984

[Tolerance of nitrefazole in alcoholics with liver disease. A 4-week placebo-controlled double-blind study].

Liver damage is one of the most common organ manifestations of chronic alcoholism. The recovery process following abstinence should not be impaired by therapy with alcohol sensitizing drugs. In a double-blind multicentre-study (controlled against placebo) the liver tolerance of Nitrefazole which is indicated as an alcohol sensitizing agent for therapy of alcoholics, was tested during the first four weeks of a planned longterm therapy. A total of 62 patients with alcoholic liver disease--demonstrated clinically and in the laboratory--were tested. The patients received 800 mg of Nitrefazole (4 capsules a 200 mg), respectively 4 placebo capsules of identical appearance, once a week in the presence of the doctor. In both treatment groups there was a significant (p less than or equal to 0.01) decline of the previously pathologically altered laboratory values, especially concerning gamma-GT, GPT, GOT. The physical and mental condition which was additionally evaluated by the doctor improved within both treatment groups. The improvement of the liver functions due to abstinence is not delayed or impaired by Nitrefazole .

Adult↗
PubMed1982

(+)-4-Dimethylamino-2,alpha-dimethylphenethylamine (FLA 336(+)), a selective inhibitor of the A form of monoamine oxidase in the rat brain.

(+)-4-Dimethylamino-2,alpha-dimethylphenethylamine (FLA 336(+)) and its N-demethylated secondary amino derivative FLA 788(+) were examined for their monoamine oxidase (MAO) inhibitory effects in the rat brain. They were found to be reversible and very selective inhibitors of the A form of monoamine oxidase in vitro and in vivo after oral administration. FLA 788(+) was 2-6 times more active than FLA 336(+) in vitro depending on the assay technique employed but the two compounds had similar potency after oral administration. Both compounds inhibited competitively the deamination of 5-hydroxytryptamine by hypothalamic mitochondria. Although the irreversible inhibitor clorgyline was 60 times more potent than FLA 336(+) in vitro, it was equipotent with FLA 336(+) and FLA 788(+) in the rat brain after oral administration. There was a high correlation between the log plasma concentration of FLA 788(+) and the MAO inhibition in hypothalamic slices. The plasma concentration of the metabolite FLA 788(+) exceeded that of FLA 336(+) after oral administration of the latter compound. Thus, the MAO inhibition produced by FLA 336(+) in vivo, appears in part to be due to the metabolite FLA 788(+).

Animals↗
PubMed1982

ColE1 copy number mutants.

A deletion mutant of the colicin E1-derived plasmid, pDMS6642, exhibited an approximately fourfold increase in copy number. We subsequently isolated hydroxylamine-induced mutants of that plasmid that had a further increase in copy number. Analysis of them suggests that the increased copy number of pDMS6642 is associated with transcriptional readthrough from a Tn3 transposon into the region of ColE1 containing information that influences plasmid replication. The hydroxylamine mutation in one copy number mutant appeared to increase the plasmid copy number by stimulating readthrough transcription from the Tn3 transposon into the ColE1 replication control region, whereas the other hydroxylamine mutation acts by another mechanism.

Bacteriocin Plasmids↗