Biomedical subjects

S Krieger

Publications and source records attributed to S Krieger.

41 records · Page 3Linked to original sources

PubMed1987

Linkage studies of Friedreich ataxia by means of blood-group and protein markers.

Friedreich ataxia (FA) is an autosomal recessive, neuro-degenerative disorder in which the pathogenetic mechanism remains unidentified despite extensive biochemical studies. Genetic-linkage studies provide an alternative approach to determining the basic defect. Linkage analysis between FA and 36 polymorphic-blood-group and protein markers has been carried out on three separate patient populations--16 families from the inbred Acadian population of Louisiana, 21 French-Canadian families from Quebec, and nine apparently unrelated British families--in an attempt to determine the chromosomal location of the disease mutation. Neither evidence of linkage to any of the markers investigated nor heterogeneity among the populations was found for any of the comparisons. The negative lod scores exclude the locus for FA from greater than 20% of the genome.

Blood Group Antigens↗

PubMed1984

Cibenzoline for treatment of ventricular arrhythmias: a double-blind placebo-controlled study.

Cibenzoline, a new class I antiarrhythmic drug, was administered to 24 patients with frequent (greater than 30/h) premature ventricular complexes. Three patients discontinued the medication because of epigastric distress before repeat ambulatory electrocardiography. Of the remaining 21 patients, 13 responded to 130 mg twice daily by more than 75% suppression of premature ventricular complex frequency and 6 additional patients responded to 160 mg twice daily during an open-label titration phase. Events of ventricular tachycardia (greater than or equal to 3 beats) were totally suppressed in 9 of 10 patients and markedly diminished in the 1 remaining patient. During a double-blind placebo-controlled crossover phase in 16 patients (21 patients minus 2 nonresponders and 3 who developed side effects), cibenzoline suppressed the number of premature ventricular complexes per 24 hours (4,075 +/- 868 to 1,758 +/- 1,089, p = 0.02), the number of events of ventricular tachycardia (31 +/- 30 to 2 +/- 0, p = 0.01) and the number of premature ventricular complex pairs (61 +/- 28 to 25 +/- 21, p = 0.01). Cibenzoline plasma concentration was 59 to 421 ng/ml in responders and higher (387, 758 and 852 ng/ml, respectively) in the three subjects with side effects (right bundle branch block in one, hypotension in one, gastrointestinal upset and central nervous system complaints in one). Cibenzoline plasma concentration correlated with PR interval (r = 0.55, p = 0.0106) and corrected QT interval (r = 0.58, p = 0.0054). Further clinical investigation of this new antiarrhythmic agent is needed.

Adult↗

PubMedDate not supplied

Cholinergic REM induction test: muscarinic supersensitivity underlies polysomnographic findings in both depression and schizophrenia.

Disinhibition of rapid eye movement (REM) sleep (e.g. shortening of REM latency, heightened REM density) is frequently encountered in patients with a major depressive disorder (MDD). Administration of cholinomimetics prior to or during sleep leads to a more pronounced advance of REM sleep in depressed patients compared to healthy controls and patients with other psychiatric disorders. The present study tested whether the cholinergic REM induction test (CRIT) with 1.5 mg RS 86 (an orally acting muscarinic agonist) differentiates patients with MDD (n = 40) from those with schizophrenia (n = 43) and healthy controls (n = 36). The most pronounced shortening of REM latency after cholinergic stimulation occurred in patients with MDD. However, a significant number of patients with schizophrenia also displayed short REM latencies (REM latency < 25 minutes) under placebo conditions and after cholinergic stimulation. REM density measures more clearly differentiated patients with MDD from those with schizophrenia. It is concluded that a subgroup of patients suffering from schizophrenia displays signs of a muscarinic receptor supersensitivity.

Adolescent↗

PubMedDate not supplied

Interleukin-6 and selected plasma proteins in healthy persons of different ages.

In the present study, interleukin-6 (IL-6) and several acute phase proteins were measured in healthy participants (23-87 years of age). A linear correlation between IL-6 and age was established with an increase of 0.016 pg/ml (0.004) per year of life. Whereas CRP remained below 0.5 mg/dl in all participants, an increase with age for fibrinogen and an inverse relation for albumin as well as transferrin were obtained. However, the increase of IL-6 did not correlate with any of these changes. IL-6 associated diseases may therefore occur more often with advancing age, but in healthy participants IL-6 does not explain the changing plasma protein pattern resembling that of an acute phase reaction.

Acute-Phase Proteins↗

PubMedDate not supplied

Cholinergic and noradrenergic neurotransmission: impact on REM sleep regulation in healthy subjects and depressed patients.

The reciprocal interaction model of NonREM- and REM sleep regulation suggests that the cycling alternating pattern of Non-REM- and REM sleep is under the control of noradrenergic/serotonergic and cholinergic neuronal networks. This model was tested in healthy humans by administration of cholinergic agonists/antagonists and noradrenergic antagonists prior to or during sleep. Cholinomimetics like physostigmine, RS 86 and galanthamine provoked an earlier onset of REM sleep, whereas subchronic treatment with scopolamine, a cholinergic antagonist, only led to a heightening of REM density. Simultaneous administration of noradrenergic antagonists with a cholinergic agonist did not provoke a more pronounced REM sleep advance. Comparative studies with the cholinergic agonist RS 86 in depressed patients, schizophrenic patients and patients with other psychiatric disorders revealed the most pronounced REM sleep response in the depressed group. The REM sleep response to cholinergic stimulation in depression did however not predict the treatment response to a differential-therapeutic strategy.

Adolescent↗